MONOGRAPHS OF 
 
 THE ROCKEFELLER INSTITUTE 
 
 FOR MEDICAL RESEARCH 
 
 No. 10 April i6, 1919 
 
 THE PATHOLOGY OF THE PNEUMONIA IN THE UNITED STATES 
 ARMY CAMPS DURING THE WINTER OF 1917-18 
 
 By 
 WILLIAM G. MacCALLUM, M.D. 
 
 NEW YORK 
 
 The Rockefeller Institute for Medical Research 
 
 1919 
 
Copyright, 1919, by 
 The Rockefeller Institute foh Medical Research 
 
 LIBRARY 
 
 NEW YORK STATE VETERINARY COLLEGE 
 
 ITHACA, N. Y. 
 
 WAVERLY PRESS 
 im WiLLMUs & WUKJNB Company 
 
 Baliimobe. U. S. a. 
 
Cornell University Library 
 RC 771.M12 
 
 The pathology of the pneumonia in the Un 
 
 3 1924 000 295 463 
 
 MONOGRAPH No. 10 
 
 THE PATHOLOGY OF THE PNEUMONIA 
 
 IN THE UNITED STATES ARMY 
 
 CAMPS DURING THE WINTER 
 
 OF 1917-18 
 
 BY 
 
 WILLIAM G. MacCALLUM, M.D. 
 
 NEW YORK 
 The Rockefeller Institute for Medical Research 
 
 1919 
 
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 ^s-^-^^ 
 
 
MONOGRAPH OF THE ROCKEFELLER INSTITUTE FOR MEDICAL RESEARCH, 
 
 NO. 10, April 16, 1919. 
 
 THE PATHOLOGY OF THE PNEUMONIA IN THE UNITED 
 
 STATES ARMY CAMPS DURING THE WINTER 
 
 OF 1917-18* 
 
 By WILLIAM G. MacCALLUM, M.D., 
 Contract Surgeon, U. S. Army. 
 
 {From the Pathological Department of Johns Hopkins University, Baltimore.) 
 
 Plates 1 to 53. 
 
 (Received for publication, August 15, 1918.) 
 
 I. HISTORICAL SURVEY. 
 
 The gathering together of great numbers of men in the United 
 States Army camps furnished conditions for an extensive outbreak of 
 measles which was quickly followed by a rather unfamiliar form of 
 pneumonia. 
 
 The Geographical and Historical Pathology of Hirsch, the volume 
 on Epidemics in Haeser's History of Medicine, and other standard 
 books that treat of the history of disease show that this is only one of a 
 great number of epidemics of pneumonia which have been recorded 
 
 * These studies have grown out of the work of two Commissions sent out by 
 the Surgeon General of the United States Army for the investigation of epidemics 
 of pneumonia among the troops. The first Commission was composed of Rufus 
 Cole, W. G. MacCallum, Oswald T. Avery, Contract Surgeons, United States 
 Army, Captains A. R. Dochez and R. A. Kinsella, and Lieutenants F. G. Blake, 
 T. M. Rivers, William C. von Glahn, J. John, and F. A. Stevens. The preliminary 
 report of the activities at Fort Sam Houston, Texas, during February and March 
 appeared in The Journal of the American Medical Association, 1918, Ixx, 1146. 
 The second Commission, which was composed of W. G. MacCallum, Contract 
 Surgeon, Captain A. W. Sellards, and Lieutenants H. M. Thomas, Jr., and 
 A. B. Lyons, worked at Camp Dodge, Iowa, during May, 1918. A brief sum- 
 mary of the activities of this Commission was presented at the meeting of the 
 American Medical Association in Chicago, in June, and appeared in The Journal 
 
 1 
 
2 PNEUMONIA IN ARMY CAMPS 
 
 since at least the 16th century. It is difficult to decide, however, 
 as to the identity of the pneumonia with what was described by con- 
 temporary writers in those long past epidemics, since they usually 
 limited themselves to the mention of a few s3rmptoms followed by a 
 lengthy discussion of their treatment of the cases. Few performed 
 autopsies or recorded descriptions that can be recognized. Never- 
 theless, their writings suggest that in many of the epidemics they 
 must have been deahng with the same condition that has existed dur- 
 ing the past winter. 
 
 In the 16th century there were many epidemics throughout Italy, 
 beginning in 1535 and sweeping over the whole peninsula. In Switz- 
 erland it was known as the malignant stitch, or Alpenstich, and by 1576 
 it had spread over Western Europe. 
 
 The attack began with a chill, pain in the head and chest, and a 
 cough which was at first dry but afterwards attended with expectora- 
 tion. The patient became delirious or fell into a stupor; loose evacua- 
 tions followed, and death occurred on the 6th or 7 th day, or if the dis- 
 ease was protracted over the 9th day the prognosis was good. Massa 
 described pleural effusions, and Coiter states that in all the cases 
 which he described he found the lungs filled with putrid blood, tur- 
 gid, and indurated, while Dodonaeus writes that abscesses were fre- 
 quent in the lungs. In the 17th century there were similar epidemics, 
 and several authors report finding serous and blood-stained eflfusions 
 in the pleura and pericardium, and the lungs in part condensed, in 
 part rendered diffluent by suppuration. In the 18th century, accord- 
 ing to Hirsch, there were still epidemics of the same "typhoid pneu- 
 monic" character in Spain, England, Italy, Switzerland, France, and 
 North America. In all these the mahgnant type of the disease is em- 
 phasized and the hepatization or purulent softening of the lungs is 
 
 of the American Medical Association (MacCallum, W. G., J. Am. Med. Assn., 
 1918, Ixxi, 704). 
 
 My grateful acknowledgment is due to the men who worked on these Com- 
 missions, for their aid, and to the various members of the staffs of the Base 
 Hospitals at these two places. Especially are my thanks due to Major L. Clen- 
 dening, of Fort Sam Houston, who furnished clinical data of most of the cases, 
 and to Major Joseph L. Miller, of Camp Dodge, who did the same for the cases 
 studied there. Major D. Glomset, who was in charge of the laboratory at Camp 
 Dodge, also afforded us every aid in his power. 
 
WILLIAM G. MacCALLUM 3 
 
 given as the characteristic anatomical feature. Morgagni describes 
 the lungs as firmly hepatized. The disease prevailed widely in France 
 in the latter part of this century. De Sauvages in 1790 describes peri- 
 pneumonia typhodes, and Deplaigne an epidemic among soldiers at 
 Valenciennes. They made postmortem examinations and found 
 suppurative processes in the lungs with effusion of pus or gelatinous 
 serum in the chest and sometimes in the pericardium. There were 
 pleural adhesions too, but the other organs were normal except for 
 swelling of the liver. In Great Britain and in Germany there were 
 also severe epidemics. 
 
 In North America there were, as described by Webster, epidemics in 
 Connecticut in 1712, 1719, 1760, and 1795. Bard tells briefly of a 
 similar epidemic at Huntington, Long Island, in 1749, and recounts 
 symptoms resembling those which we have seen recently, but he made 
 no dissections. I have not been able to associate these epidemics 
 with the gathering of troops during the Revolutionary War or to 
 find any papers referring especially to this period. 
 
 In 1812, however, there began a great epidemic which, starting in 
 Canada, spread throughout the Northern States and finally into the 
 South. There is a great deal of literature about this, and the Medical 
 Repository and the American Medical and Philosophical Register made 
 a special point of gathering together communications and essays re- 
 lating to it. There is also a book by James Mann, Hospital Surgeon 
 of the Army, published in 1816 (Medical Sketches of the Campaigns of 
 1812, 1813, and 1814) which gives a good description of the condition, 
 including a few postmortem observations. From these it may be 
 learned that some of the soldiers died with extensive pleural effusion, 
 sometimes of thick pus, as in the case of one man whose pleura was 
 drained by an incision between the ribs, and sometimes of a thick yel- 
 lowish whey-colored fluid, while a membrane of coagulated lymph fined 
 the cavity of the thorax. In one case the limgs were dark purple, but 
 on incision thick pus could be forced by compression out of the air cells. 
 In another the lungs were contracted, compact, tough, and almost des- 
 titute of air vessels. Another showed the lung large, hard, and ad- 
 herent to the upper part of the cavity. It appeared like the liver, 
 tender and easily lacerated with the fingers, and entirely destitute of 
 the spongy texture peculiar to healthy lungs. In its superior part 
 
4 PNEUMONIA IN ARMY CAMPS 
 
 adjoining the clavicle and near the trachea was a large sphacelus, part 
 of which had been coughed up. Pus was by compression squeezed 
 out of the air cells. In another case the lung was adherent on aU 
 sides, and specks of pus were found throughout it, but no abscesses. 
 
 Still another case presented a lung in which a small portion had come 
 to resemble the liver, and the cells contained pus. The other lung 
 exuded pus on every incision. It was not much dissimilar to a honey- 
 comb, if filled with pus. The last, or eleventh case revealed three 
 pints of limpid glutinous serum resembling whey in each cavity of the 
 thorax. The right lung was contracted to half its natural size. The 
 upper part was consolidated and hardened, feeling and appearing like 
 a piece of heart boUed. Adhesions had formed to the spine, ribs, 
 clavicle, and pericardium. The lobe was so much drawn to the spine 
 that no adhesion existed between it and the ribs of the anterior part 
 of the thorax. In the upper part of the lobe immediately under the 
 clavicle there was an abscess as large as a goose egg. There were 
 found adhering to the pleura and lungs a membrane of coagulated 
 lymph and some similar thick pieces resembling what is commonly 
 called mother of vinegar. The left lobe appeared httle diseased, but 
 on cutting into the substance drops of pus were squeezed out of its 
 cells. While one or two of these cases appear to have been instances 
 of lobar pneumonia, the others in which there was such extensive 
 pleurisy and from the lungs of which drops of pus could be squeezed 
 resemble closely the cases found in the present day epidemic. 
 
 The descriptions of the clinical symptoms given by Mann, Bard, 
 Eights, Matson Smith, Valentine Mott, McBride, and others agree 
 closely, but by far the best is given by James Low who described 
 the beginning of the epidemic in Albany in October, 1812. 
 
 "The onset is with a chill, prostration and a feeble pulse, horror and distress 
 from pain in the head, back, and extremities. The tongue is furred, the breath- 
 ing insupportably laborious even when the pain in the chest is not severe, and 
 every muscle concerned in this function ceases to act until goaded on by voHtion. 
 When the pain is acute the anguish is inexpressible. Every cell in the lung 
 seems infarcted and weighed down by the load. 
 
 "Restlessness, distressing dreams, sudden frights, and starting from sleep at- 
 tend most cases. Many are unable to endure the horizontal posture from a 
 sense of suffocation which attends that position. Coma and delirium ferox are 
 frequent symptoms and there are aphthae and ulcers in the throat in some cases. 
 
WILLIAM G. MacCALLUM 5 
 
 I 
 
 The disease sometimes terminates in scarlet fever, measles, or an anomalous 
 rash, all of which prevailed, as was the case in other countries where the same 
 epidemic has raged. Morgagni, Coiterus, and Wierus describe the same in Italy 
 and Germany, Cleghorn in Minorca, Sydenham, Huxham, and Home in England." 
 
 Low saw gangrene of the leg in one case. Hosack also mentions 
 autopsies in this epidemic in which he found an overloaded state of the 
 vessels of the lungs. A large effusion of serum and sometimes purulent 
 matter and the adhesions between membranes covering the limgs and 
 those hning the chest show that there has been inflammation of the 
 lungs. It was, he decides, a local inflammation with a typhous state 
 of the whole system from which he refers to it as peripneumonia 
 typhodes. 
 
 Mann, in another paper written from Plattsburg, states that the 
 most prevalent disease was measles, which predisposed those who had 
 it to pneumonia. He gave once more a description of the lungs which 
 were inflamed with adhesions to circumjacent parts, with the surface 
 covered with yellowish gelatinous semiputrid extravasation. The 
 spongy texture of the lungs was lost and the organ assumed the com- 
 pactness of the liver. 
 
 McReynolds in describing an epidemic among troops at Black Rock 
 gives similar details of autopsies, and so does Hudson concerning an 
 epidemic on the Niagara Front. Hudson was especially interested in 
 the extension of inflammation through the diaphragm to the surface 
 of the liver. A similar affection with pleurisy with serous effusion 
 and pulmonary changes was observed in the New York Hospital in 
 January, 1813. 
 
 After the disease had raged among the troops and inhabitants of 
 northern New York it appears to have occurred with especial intensity 
 in Dutchess County, East Chester, and West Chester, as well as in 
 New York City and Long Island, but there were also many cases in 
 Coimecticut, Vermont, and Maine. Nowhere are the pulmonary 
 changes minutely described, but it is evident from the occasional clear 
 descriptions of definite hepatizations and the vague descripition in 
 other cases of congestion alternating with abscesses or with a form of 
 consolidation from which one could squeeze pus from the bronchi 
 that most of it perhaps was not definite lobar pneumonia but prob- 
 ably a form of bronchopneumonia with extensive pleural exudate. It 
 
6 PNEUMONIA IN ARMY CAMPS 
 
 died out in these states in 1815, but passed into the Southern States 
 and persisted until 1826. 
 
 Although there were many epidemics in various parts of Europe at 
 this time I have not been able to learn so far that this type of disease 
 was prominent in the armies engaged in the Napoleonic Wars. 
 
 From 1815 to 1862 there were occasional epidemics. Little in- 
 formation appears to be available regarding the troops during the 
 Civil War. Bartholow described the occurrence of measles and its 
 sequelae in the camps, and Woodward gives statistical information 
 showing that measles was prevalent, that pneumonia followed it, and 
 that the mortahty was considerable, but these conditions were greatly 
 overshadowed by the colossal prevalence of typhoid fever and dysen- 
 teric disease, and Woodward's attention seems never really to have 
 reached pneimionia. The following is abstracted from this history. 
 
 Measles. — During the years covered by statistics there were 67,763 cases of 
 measles, with 4,246 deaths among white troops, with a mortality of 6.27 per 
 cent. Most of this mortality was due to secondary pulmonary affections. Many 
 deaths were referred to pneumonia without mentioning measles. Per 1,000 
 the average annual rate was 30.41, the maximum 77.57 in the 1st year, the mini- 
 mum 1.98 during the last year. Many regiments suffered at recruiting stations. 
 
 In colored troops there were 8,555 cases, with 931 deaths, or 10.88 per cent 
 of fatal cases. 
 
 In the Confederate Army of the Potomac there were 8,617 cases in an army 
 of 58,360 during July, August, and September, 1861, 430 cases in October, 
 241 in November, 79 in December, 34 in January, 1862, and 8 in February. 
 A succession of epidemic waves involved susceptible men of successive additions 
 to strength of command. 
 
 As the new men came within the influence of the contagious focus the disease 
 spread, giving a sudden elevation to the line of prevalence which thereafter feU 
 until fresh additions occurred with a corresponding rise in its level. 
 
 Among the white troops the line of prevalence shows a seasonal influence as 
 well as that due to the aggregation of susceptible individuals. The warm season 
 operated favorably on these troops. The disease was especially severe among 
 negroes, being characterized by bronchial inflammation, pneumonic congestion, 
 and solidification, laryngeal congestion and edema, and sometimes affections of 
 the intestinal mucous membrane. 
 
 CHnical records of measles show a return to duty 3 or 4 weeks after onset, 
 but in many cases the stay in the hospital was prolonged for as many months 
 by the continuance of bronchial inflammation or the supervention of broncho- 
 pneumonia or diarrhea. In some cases the specific agency manifested its virulence 
 
WILLIAM G. MacCALLTJM 7 
 
 by a dark purple color of the eruption and symptoms of internal congestion. 
 In general the point of interest is the consecutive disease. Sometimes pneu- 
 monic congestion was suddenly developed by exposure while the skin was af- 
 fected, but more frequently pulmonary disorders, including consumption, ap- 
 peared to be engrafted on the patient during convalescence. Laryngitis in some 
 cases caused sudden death, and in others a temporary or even permanent aphonia. 
 Cerebral meningitis sometimes occurred, and intercurrent or sequent attacks of 
 erysipelas were common. Conjunctivitis was a frequent sequel and deafness 
 followed the invasion of the middle ear by way of the Eustachian tube. Occa- 
 sionally the ear became involved in the suppuration of the glands in its neighbor- 
 hood. Edema of the feet, orchitis, and ischiorectal abscess including fistula in 
 ano were among the sequelas. 
 
 "Recruits from the city are more likely to have passed through the disease in child- 
 hood than those from the rural districts. City regiments are therefore to be preferred in 
 this connection. When the call to service is urgent this becomes a secondary matter. 
 The liability to disease under exposure to its causes must be accepted as a part of the 
 danger to be faced. Measles will thus continue to be a subject of interest and anxiety 
 to army medical men until the discovery of a means of protection against it independent 
 of subjection to its influence in previous epidemics." 
 
 Later (page 788) he suggests the propriety of inoculation. 
 
 Pneumonia. — "61,202 cases of pneumonia occurred among the white troops during 
 the war, with 14,738 deaths, so that the importance of pneumonia as a destroyer of life 
 in our camps and hospitals can hardly be overestimated. The postmortem records of 
 cases reported as pneumonia show that death in the majority of instances resulted not 
 alone from hyperemic or inflammatory processes in the pulmonary tissues, but from 
 these in conjunction with similar processes affecting particularly the pleural membranes, 
 bronchial tubes, and pericardium. With the production of these congestive or inflam- 
 matory results the malarial, typhous, and tuberculous cachexias and the specific cause 
 of measles were apparently often connected." 
 
 Of 435 cases recorded after postmortem examination, 300 were distinguished 
 as lobar pneumonia, 135 as secondary or catarrhal inflammation. Of the 135 
 cases, 101 were associated with measles. These cases are inadequately de- 
 scribed and as a rule it is merely stated that parts of the lung were hepatized, 
 and in a few instances thickening with softening of the bronchi was mentioned. 
 Pleurisy with effusion was common and there is slight mention of laryngitis. 
 Pericarditis was present in a few cases but was by no means so frequently associ- 
 ated with secondary pneumonia as with the acute lobar cases. Pleurisy as such 
 seems to have been recorded in 31,852 cases during the war, but although 590 
 were fatal only 45 were observed and described post mortem and of these 6 were 
 connected with measles. 
 
 Of the cases of bronchopneumonia following measles the lungs 
 of three have been preserved in the Army Medical Museum in 
 
8 PNEUMONIA IN ARMY CAMPS 
 
 Washington, and Dr. Lamb was kind enough to allow me to study 
 them and even to take portions for microscopic study. They are 
 from Case 50 (Medical and Surgical History of the War of the 
 Rebellion, Vol. I, Part 3, Medical Volume, page 789), Case 105 
 (page 794), and Case 134 (page 798). All these cases were observed 
 by Surgeon E. Bentley, U. S. Voltinteers, Third Division Hospital, 
 Alexandria, Virginia. 
 
 The history in Case SO states that Private J. B. Talbot, aged 23, was ad- 
 mitted Feb. 13, 1864, with pleuropneumonia following measles and died Feb. 29. 
 Postmortem examination showed that the lower lobe of the right lung was hepa- 
 tized, red, and presented on section a number of small superficial abscesses. The 
 pleura was thickened (Specimen 345, now renumbered 7,792). The lung is cov- 
 ered with fibrinous exudate and most of it is spongy in texture, but it contains 
 some distinct firm nodules which are branched at times. 
 
 Section of this lung no longer stains well, but the outlines of cells 
 may be discerned. There is in the section a patch of consolidation 
 and then one of air-containing tissue with two small foci of consolida- 
 tion. These have central bronchioles which contain exudate and have 
 lost their epitheHum. The walls are very thick and infiltrated with 
 mononuclear cells and are penetrated by many blood vessels distended 
 with blood. The adjacent alveolar walls are similarly infiltrated and 
 contain dense plugs of fibrin with desquamated epithelium. 
 
 The larger area of consolidation shows several bronchi with the 
 same change. The walls of a rather large one are especially infil- 
 trated. The more peripheral alveoH have dense contents of fibrin and 
 epithelium. In the more central part of the patch the tissue is dis- 
 integrated and full of very small broken cells, possibly leucocytes. 
 There is a mass of granular material at one spot resembhng bacteria. 
 
 With Weigert's method the bacteria stain quite sharply and great 
 masses of definite streptococci are found in the midst of the necrotic 
 area. No other organisms were found. 
 
 This appears to have been a case of streptococcal bronchopneumonia 
 in which certain areas of consolidated tissue have become necrotic in 
 mass and contain large clumps of bacteria. 
 
 The history of Case 105 is as follows: Private Jacob Maust, aged 20, was ad- 
 mitted Mar. 26, 1864, moribund from pneumonia after measles. He died on the 
 28th. 
 
WILLIAM G. MacCALLTJM 9^ 
 
 On postmortem examination it was found that the left pleural cavity contained 
 a pint of serum and the lung was coated with thin pasty lymph, the lower lobe 
 being partly hepatized. 
 
 Specimen 343, now numbered 7,790, shows the following. The 
 pleura is greatly thickened and edematous with wide interlobular septa. 
 
 The lymphatics are enormously wide and are distended with cell 
 masses. In these and on the surface of the pleura there are large 
 numbers of streptococci in distinct chains which stain well. No in- 
 fluenza bacilli could be demonstrated. The bronchi are distinctly 
 thickened. New blood vessels in great numbers have formed in their 
 walls, the epithelium is lost, and streptococci occur in their purulent 
 contents. There is collapse, but not much consolidation about them. 
 
 This appears to be a case of interstitial bronchopneumonia with 
 lymphatic transportation of the streptococci. 
 
 The history of Case 134 is as follows: Private John H. McMichael, aged 19, 
 was admitted Mar. 11, 1864, with pleurisy and laryngitis, secondary to measles. 
 He died on the 23rd. 
 
 On postmortem examination the larynx and trachea were found to be in- 
 flamed and filled with tenacious mucus; right lung collapsed and friable. Lower 
 lobe thickly coated with pseudomembrane. Left lung slightly congested (Speci- 
 men 342, now numbered 7,789). 
 
 The lung shows a thin layer of fibrin; the pleural surface and the 
 pleura itself are markedly thickened. Interlobular septa are promi- 
 nent. At the base of the upper lobe there is a small area of diffuse 
 consoUdation. The rest is air-containing except for numerous small 
 nodules of consolidation with central bronchioles. 
 
 Sections show numerous small bronchi filled with debris of leuco- 
 cytes. The epithelium is desquamated and the underlying tissue 
 necrotic. The alveoli round about are filled with fibrin and cells, 
 some of which are leucocytes. There is no great interstitial change 
 in most of the lung. Definite cocci in pairs and short chains are found 
 in the bronchioles. In o\her places bronchial and blood vessel walls 
 are markedly infiltrated with cells. The intervening lung substance 
 is air-containing. 
 
 This is a focal streptococcal pneumonia in which there is little 
 interstitial change but chiefly small peribronchial foci of lobular 
 pneumonia. 
 
10 PNEUMONIA IN ARMY CAMPS 
 
 It is evident that in these three cases we have representatives of the 
 types of streptococcal pneumonic lesion which occur in the epidemic of 
 today. The first case is one of interstitial bronchopneumonia with 
 large areas of necrosis, the second belongs to the same type but with- 
 out the necroses, while the third is an earlier stage with much less in- 
 terstitial change. It is especially interesting that after 54 years in 
 alcohol the streptococci still stain brilliantly. 
 
 Surgeon Ira Russell also reported that there had been 784 cases of 
 pneumonia at Benton Barracks, Mo., in 1864, of which 156 died. 
 Beside these there were 675 cases of measles, of which 130 died of 
 pneumonia. He distinguishes congestion, typhoid, and pleuropneu- 
 monia. There is a marked difference in the morbid appearance of the 
 lungs in the pneumonia following measles from their appearance in 
 pneumonia produced by other causes. Hepatization is less marked, 
 the lung tissue oftener edematous or filled with serosanguineous fluid 
 and containing a sufficient quantity of air to make it float on water. 
 When pressed between the fingers a large quantity of bloody serum 
 exudes. The lung frequently passed from this edematous condition, 
 without going through the stages of red and grey hepatization, into 
 that of purulent infiltration. 
 
 Since the Civil War other epidemics of pneumonia have been de- 
 scribed, but it is generally difficult from the clinical descriptions to 
 determine the nature of the disease, and practically none of the 
 authors in this country appear to have recorded postmortem 
 examinations. 
 
 In Europe many such epidemics were briefly described also (Lav- 
 eran, Bard), without adding perceptibly to the comprehension of the 
 disease. But with Bartels there began a more accurate anatomical 
 study of the peculiar form of bronchopneumonia which follows 
 measles, whooping cough, diphtheria, and perhaps other acute infec- 
 tious diseases. 
 
 Delafield in various publications in this country has given clear 
 descriptions of the pecuHarities of this form of bronchopneumonia 
 in children and in adults, emphasizing its interstitial character and the 
 lateral involvement of the alveoli which adjoin the bronchioles to- 
 gether with the accompanying atelectasis. His understanding of the 
 contrast between this type of pulmonary affection and the sort of 
 
WILLIAM G. MacCALLUM 11 
 
 exudative process which follows the aspiration of infected materials 
 into the bronchi, or the other examples of terminal patchy pneu- 
 monia characterized by the filling of the alveoli which are connected 
 with the infected bronchioles with an exudate of polymorphonuclear 
 leucocytes, is satisfactory and his descriptions form a model of con- 
 ciseness. At this time there was a prevalent doctrine which distin- 
 guished between croupous or lobar pneumonia in which there is an 
 exudate of leucocytes and fibrin, and catarrhal or bronchopneumonia 
 in which fibrin was less in evidence and the alveoli contained large 
 mononuclear cells mixed with others. This seems to be an inade- 
 quate basis for the anatomical distinction, and more recent writers 
 have not accepted it, although these terms are still used. 
 
 Since Bartels' paper, a series of German publications has appeared, 
 describing more clearly the interstitial form of bronchopneumonia in 
 children after diphtheria, measles, and whooping cough, and from an 
 anatomical point of view these leave little to be desired, although 
 none except those of Diirck and Finkler are concerned with the bac- 
 teriology of the disease. From these are derived no doubt the de- 
 scription found in most of the text-books, although the description 
 given by Orth is evidently from his own observations. Wagner, 
 Jiirgensen, Aufrecht, Kromayer, Koester, Wygodzinski, Diirck, 
 Honl, Steinhaus, Hart, Jochmann and Moltrecht, and Hecht have 
 all contributed papers which are easily accessible. 
 
 These papers agree closely in their descriptions of the pathological 
 anatomy of this form of bronchopneumonia, the best of which are those 
 of Steinhaus and Hecht. Wygodzinski distinguishes lobular and con- 
 fluent forms in which the alveoli are filled with a fibrinous and leuco- 
 cytic exudate, from peribronchitic inflammation, but he also recog- 
 nizes combinations. Honl points out the resemblance of the small 
 firm nodular consolidation in these lungs to miliary tubercles, but in- 
 sists that tuberculosis is not of frequent occurrence after measles, and 
 that the common impression that it is, may depend upon the erron- 
 eous interpretation of these peribronchial nodules as tubercles. He 
 saw the peculiar epithelial giant cells upon which later writers have 
 laid stress. 
 
 Steinhaus reviews the earlier German literature, gives a clear de- 
 scription of the pulmonary lesions, and summarizes his paper as 
 follows : 
 
12 PNEUMONIA IN ARMY CAMPS 
 
 Measles pneumonia is in the beginning not a lobular inflammation but ap- 
 pears in minute foci, of which several are found in a lobule. It is never catarrhal, 
 since fibrin is abundantly present. 
 
 The focal consolidations result from a primary bronchiolitis and peribronchiolitis 
 through a propagation of the inflammatory irritant by way of the lymph vessels. 
 There are several types of lesions, (o) The acute focus with exudation into the 
 alveoli. This may arise by extension of the inflammation from the bronchioles 
 to adjacent alveoli which do not belong to its respiratory district or by propaga- 
 tion along its lumen to its own alveoli. In the zone of fresher exudate fibrin is 
 always present. (6) The more chronic focus, proceeding in the form of an inter- 
 stitial peribronchitis with advanced changes in the interstitial tissue but no 
 exudation in the alveoli. 
 
 This change appears to be related in its origin to the peribronchial 
 and perivascular lymph follicles. The interstitial change arises very- 
 early in measles pneumonia and distinguishes it from the croupous 
 form. The distinction between the acute and the more chronic foci 
 of pneumonia lies in the presence of a leucocytic infiltration in the 
 first, a lymphatic infiltration in the second. He apparently saw no 
 giant cells, but Hecht who also studied the lungs of children lays 
 especial stress on their presence in his paper which has the title 
 "The giant cell pneumonia of children." This is a form of pneu- 
 monia which occurs only in young children after measles and whoop- 
 ing cough in connection with a hypertrophic bronchitis. The giant 
 cells arise from the epithelium either by incomplete division or by 
 coalescence. They could never be produced experimentally in rab- 
 bits by intrabronchial injections of staphylococci or pneumococci, 
 but could be imitated closely in animals injected intratracheally with 
 various metallic salts (especially silver nitrate and copper sulphate) 
 or ammonia. Karsner and Meyers described and discussed a similar 
 case in a child and reference will be made to this later in connection 
 with one of our cases. 
 
 All these papers have dealt with children and I have found little 
 referring to such bronchopneumonia in adults. Delafield recognized 
 it in adults, but his attention was chiefly directed to the disease in 
 children. 
 
 Mathers describes an epidemic of pneumonia occurring in Chicago 
 during the season 1915-16 in which he isolated Streptococcus pyo- 
 genes in a majority of instances. His description of the lung refers to 
 
WILLIAM G. MacCALLXJM 13 
 
 the gross appearance only. There were extensive pleuritis and peri- 
 carditis and the cut surface of the lung was smooth and mottled grey- 
 ish red and dark red. The greyish areas varied in size and consist- 
 ency, some being firm and dry while others were moist and viscid. 
 They had no relation to bronchi and were sharply outlined like in- 
 farcts. Other dark red areas were soft and hemorrhagic. The de- 
 scription is too indefinite to allow one to recognize the condition with 
 certainty. 
 
 During the present war, epidemics have been studied in the north 
 of France by Hammond, Rolland and Shore, and at Aldershot in 
 England by Abrahams, Hallows, Eyre, and French. They describe a 
 purulent bronchitis which is fatal and from which they isolated the 
 influenza bacillus from the sputum in most of the cases. They found 
 other organisms at times, including the pneumococcus, streptococcus 
 (five times), D. catarrhalis, staphylococcus, M. tetragenus, etc. Pleu- 
 risy appears not to have been common and mention is made of only 
 eight cases in which a clear yellow fluid had accumulated in the 
 pleural cavity. The bronchi are filled with pus and there is a peri- 
 bronchiolitis. Photographs of sections of the lungs show the peri- 
 bronchial infiltration distinctly, and the anatomical description which 
 is given with these makes it seem evident that the lesion is practically 
 the same as that which we are about to describe for the epidemic in 
 this country. The lack of pleurisy is one great point upon which 
 they differ from our cases, and the second is in the predominant role 
 of the influenza bacilli. 
 
 In a letter dated June 22, 1918, from a hospital in France, Dr. 
 Archibald Malloch writes me concerning such an epidemic in which 
 he had studied nine cases at autopsy. He says nothing of empyema 
 in these cases. • ' ' ' 
 
 "Clinically the cases were generally like capillary bronchitis, and as a rule 
 no dulness could be made out, although sometimes this was present. There were 
 marked dyspnea and cyanosis. At autopsy there was often no consolidation of 
 any extent but grey-white pus was found even down to the finest bronchioles 
 (swarming with B. influenzcB s.nd there obtained in pure culture). At other times 
 there were small areas of atelectasis with tiny yellowish abscesses in them. On 
 the other hand, some of the lungs showed confluent bronchopneumonia. Two of 
 these cases showed an endocarditis with vegetations, from the cultures of which 
 Major Rhea grew B. influenza in pure culture." 
 
II. THE EPIDEMIC IN THE UNITED STATES ARMY CAMPS, 
 
 The conditions existing in these ancient epidemics have in a sense 
 been repeated on a magnified scale in the course of the assembling 
 of the troops from all parts of the United States in the present war, 
 and the results with respect to disease of the respiratory organs have 
 been much the same. It is obvious that the sanitary conditions 
 surrounding the cantonments and camps have been extremely good as 
 far as forms of disease which were especially destructive in the Civil 
 War and in many other wars are concerned, and the result is that 
 with the aid of vaccination against typhoid fever, paratyphoid, and 
 smallpox, those diseases have not appeared. Even diphtheria is now 
 practically under complete control. But sanitation and preventive 
 medicine are as yet helpless against measles and pneumonia, and 
 therefore these diseases have swept through the well ordered camps as 
 they did in 1812. 
 
 The draft brought together large numbers of men of ages from 21 to 
 31 years from all conditions of life. Many of them had lived in cities, 
 accustomed all through their lives to close intercourse with the 
 densest populations and these had passed through all the ordinary 
 diseases of childhood and had acquired immunity. Others, however, 
 and especially perhaps those from the South, had lived in remote rural 
 districts under entirely different conditions with but little contact 
 with any great number of other people. These came to the camps un- 
 protected from any disease except smallpox and typhoid fever. The 
 compulsory vaccination conferred this protection and eliminated these 
 diseases from the army in a way which could not be paralleled by any 
 measures of sanitation which aimed at their exclusion by even the 
 most rigid control of all the recognized channels of infection. 
 
 To the remaining acute exanthematic diseases and to respiratory 
 infections these men were highly susceptible. To other infections 
 they were also susceptible, but these have assumed such a prominent 
 place in the history of disease in the camps that the rest appear 
 rather insignificant. 
 
 14 
 
. WILLIAM G. MacCALLUM 15 
 
 It must not be stated that the respiratory diseases occurred exclu- 
 sively in the troops of rural origin, since they gained such virulence as 
 to affect all, but it does seem clear that immunity acquired by 
 exposure and infection in early life has played a great part in pro- 
 tecting the men of some of the camps from disease. 
 
 Emphasis should be laid, I think, upon the importance of 
 measles in the inception of this epidemic. Measles has prevailed to 
 an extraordinary degree in many of the camps in the South, and 
 there too have arisen the greatest epidemics of bronchopneumonia. 
 When pneumonia taken as a whole and including lobar and all 
 forms of bronchopneumonia is plotted out on a map, as was done 
 in the office of the Surgeon General, so as to show the camps in 
 which the greatest number of cases occurred, as black circles, and 
 especially when the position of these camps is indicated according 
 to the district from which they drew their troops, all the black 
 circles are in the South. Any such statement is necessarily somewhat 
 inaccurate. Measles is not absent in the northern camps nor is 
 pneumonia. Lobar pneumonia caused by the pneumococcus, which no 
 one suspects of being especially a sequel of measles, probably occurs 
 in much the same proportion throughout all the camps. But the 
 form of bronchopneumonia which has for years been recognized as a 
 common sequel of measles has appeared in enormous proportions in 
 the southern camps in which hundreds and even thousands of cases 
 of measles developed. It is true that this type of pneumonia in these 
 camps frequently occurred in patients who had not had measles, and 
 it is clear that it is due to some second infection and not to the measles 
 itself. It was not altogether surprising, therefore, to find large epi- 
 demics of the same type of bronchopneumonia arising later in northern 
 camps where measles had not existed to a great degree and in troops 
 which had not been in contact with the few cases of measles which 
 were isolated in distant barracks. 
 
 Briefly stated, the great epidemic seems to be an epidemic of 
 bronchopneumonia, with measles as the most important predisposing 
 cause, but the bronchopneumonia, which itself is due to a secondary 
 infection, later arose independently of measles in individual cases and 
 in other camps when the agent which caused the secondary infection 
 became virulent enough to give rise to the disease independently. 
 
16 PNEUMONIA IN ARMY CAMPS 
 
 The following study of the forms of pneumonia which prevailed 
 makes no attempt to outline the extent of these diseases in the various 
 camps, since that information will be available from the reports of the 
 office of the Surgeon General. Nor is it intended to trace the course 
 of the various epidemics or to give statistics of the incidence of pneu- 
 monia or the number of deaths caused by it. Instead it is an attempt 
 to analyze the character of the respiratory diseases observed at Fort 
 Sam Houston, Texas, during February and March, and at Camp 
 Dodge, Iowa, during May, from the standpoint of the student of 
 their etiology and pathological anatomy. 
 
 In the study of the respiratory disease in these camps a consistent 
 plan was followed. In a large number of cases observed cHnically, cul- 
 tures were made from the sputum, swabs from throat, and cultures from 
 the circulating blood and fluid aspirated from the pleural cavities. 
 These were, of course, of great importance in diagnosis and threw much 
 Hght upon the condition found at autopsy. The most satisfactory 
 information was derived, however, from the cases in which the bac- 
 teriological results could be confirmed and controlled by cultures 
 from the tissues at autopsy, and in as far as these cases were concerned 
 we endeavored to tabulate the records in such a way as to show at once 
 the results of cultures made during life and after death from all these 
 sources. It was interesting to find that repeated cultures made dur- 
 ing life and after death sometimes showed the disappearance of one 
 organism and its replacement or overgrowth by another. Our in- 
 formation is sufficiently complete for this purpose in about 49 cases 
 of pneumonia which are therefore given in Table I. The cases which 
 were studied chnically only need not be included, since they have 
 been discussed in other papers. 
 
 It will be seen from this table that a great variety of lesions 
 and several types of infection are represented here with various com- 
 binations. In general, analysis of the cases shows that there were 
 two main forms of infection, that in which the pneumococcus was the 
 etiological agent and that in which this part was played by Strepto- 
 coccus hcemolyticus . 
 
 The influenza bacillus was frequently found in the sputum and 
 occasionally in the lungs and pleural fluid. It was always associated 
 with the streptococcus, however, and it is difficult to assign it a pre- 
 
Autopsy 
 No 
 
 Antecedent disease. 
 
 Clinical bacteriology. 
 
 Pleural 
 involve- 
 ment. 
 
 Complications. 
 
 
 
 Sputum. 
 
 Blood. 
 
 Pleural fluid. 
 
 Heart's bio 
 
 Interstitial bronchopneumonia 
 
 14 
 IS 
 16 
 32 
 34 
 37 
 39 
 41 
 49 
 167 
 171 
 174 
 178 
 184 
 191 
 193 
 
 Measles. , 
 
 Measles 
 
 Measles 
 
 Measles 
 
 Measles 
 
 Measles 
 
 Scarlatina 
 
 Measles; scarlatina. 
 
 Measles. . 
 Measles. 
 
 SH. 
 
 SH.. 
 
 SH., 
 
 SH.' 
 
 SH.. 
 
 BI' 
 
 BI. 
 BI. 
 
 StA. BI. 
 SH 
 
 Pnlll. StA. 
 
 Neg. 
 
 Neg. 
 Neg. 
 SH.. 
 
 SH. 
 
 Neg 
 
 Neg 
 
 Neg 
 
 SNh. Neg. 
 
 SH. 
 
 SNh. 
 
 SH. 
 
 Empyema. , 
 
 Empyema. 
 
 Empyema. 
 
 Empyema. 
 Empyema. 
 Empyema . 
 Empyema. 
 Empyema. 
 Empyema. 
 Empyema . 
 Empyema . 
 
 Empyema. 
 
 Pericarditis . 
 
 Acute nephritis. , 
 
 Ulcerative laryngitis. 
 Ulcerative laryngitis. 
 
 SH.. 
 SH., 
 
 SH.. 
 Neg., 
 SH.., 
 SH.. 
 SH.. 
 
 SH. 
 SH. 
 
 SH. 
 SH. 
 
 
 
 
 
 
 
 Interstitial bronchopneumonia and lobular 
 
 24 
 
 
 
 
 
 
 
 
 29 
 
 
 SH 
 
 Neg 
 
 
 
 
 SH 
 
 30 
 
 
 
 
 
 
 
 35 
 
 
 
 
 
 Empyema. . 
 
 Acute nephritis 
 
 SH 
 
 58 
 
 
 
 
 
 SH 
 
 176 
 
 
 
 Neg 
 
 SH 
 
 Empyema . . 
 Empyema. . 
 Empyema. . 
 Empyema. . 
 
 Pericarditis; abscess. 
 
 
 181 
 
 Bronchitis; diphtheria 
 
 
 SH 
 
 SH 
 
 192 
 
 
 SH. 
 SH. 
 
 BI.. 
 
 
 
 Ulcerative laryngitis . 
 
 SH 
 
 205 
 
 Measles. . . 
 
 BI.. 
 
 NCB 
 
 
 SH 
 
 
 
 
 
 
 
 Lobular pneumonia. 
 
 20 
 
 
 
 
 
 
 
 
 26 
 
 Measles 
 
 SH. 
 
 
 
 Empyema . . 
 Empyema. . 
 
 Pericarditis 
 
 
 SS 
 
 
 SH. BI.. 
 
 Neg 
 
 SH 
 
 SH. 
 
 Septicemia 
 
 SH 
 
 56 
 
 
 
 187 
 
 Rubella 
 
 SH. StA. 
 StA. BI.. 
 
 Neg 
 
 
 
 
 SH 
 
 192 
 
 
 Neg 
 
 
 
 Ulcerative laryngitis. 
 
 SH 
 
 195 
 
 
 
 
 Empyema . . 
 
 
 
 
 
 
 
 
 
 
 Lobar pneumonia. 
 
 18 
 
 
 
 
 
 
 
 PnlV.... 
 
 19 
 
 
 
 
 
 Empyema. . 
 
 Pericarditis 
 
 
 25 
 
 
 Pnll.. 
 SH. 
 
 BI.. 
 
 Pnll 
 
 
 
 
 33 
 
 
 PnlV 
 
 SH 
 
 
 
 SH. BI . 
 
 36 
 
 
 
 Empyema . . 
 
 Acute pericarditis . . . 
 
 
 40 
 
 
 
 
 
 
 
 45 
 
 
 
 
 
 
 Endocarditis 
 
 Pnl {valv 
 
 46 
 
 
 SH. 
 
 PnHa 
 
 Pnl. 
 
 Pnl. 
 BI.. 
 BI.. 
 
 Pnl 
 
 Pnlla 
 
 SH. Pnl 
 
 Neg 
 
 Empyema . . 
 
 SH 
 
 51 
 
 
 
 Pnlla. . . 
 
 186 
 
 
 
 Empyema. . 
 
 
 Pnl 
 
 188 
 
 
 
 
 
 Acute nephritis 
 
 
 
 
 
 
 
 
 
 
 Interstitial bronchopneumonia and lobar p 
 
 21 
 
 
 
 
 
 Empyema. . 
 
 
 SH. Pnl\ 
 
 23 
 
 
 
 
 
 Empyema. . 
 
 
 SH 
 
 31 
 
 
 
 
 PnlV (lung)... 
 SH 
 
 Empyema. . 
 
 
 SH 
 
 50 
 
 
 SH. BI. . 
 Pnlla. BI.. 
 Pnll 
 
 Neg 
 
 Pnlla 
 
 
 
 SH 
 
 180 
 
 
 
 
 Ulcerative laryngitis. 
 
 SH 
 
 196 
 
 
 Pnll 
 
 
 
 
 
 
 
 
 
 
 
 * SK. indicates Streptococcus heemolyticus; StA., Staphylococcus aureus; SNb., non-heraolytic streptococcus; BI., Bacillus influe; 
 Pneumococcus Types U, III, and IV. 
 
WILLIAM G. MacCALLUM 17 
 
 dominant part in the causation of the pneumonia. In general the 
 pneumococcus of whatever type produced lobar pneumonia, and the 
 streptococcus either what we shall describe as interstitial broncho- 
 pneumonia, or another lesion to which for convenience we assign the 
 name lobular pneumonia.' The exact biological nature of this strep- 
 tococcus and its identity in different camps are still subjects which 
 are actively discussed. It seems to be the same wherever it has 
 been found, but it will require time to determine whether there are 
 several strains at work. Indeed, from many camps there come reports 
 of numerous cases due to a non-hemolytic streptococcus. All these 
 important points must be settled by further study, which must also 
 decide the significance of the influenza bacillus, staphylococcus, and 
 other organisms in the production of the disease. Our own expe- 
 rience has led us to beheve that a fairly constant hemolytic strepto- 
 coccus is the important factor. 
 
 In practically all the cases of streptococcus infection there appears, 
 if there is sufficient time before death, a serofibrinous or fibrino- 
 purulent pleurisy. This sometimes persists as an empyema even after 
 the earher pulmonary lesions from which it originated have com- 
 pletely or almost completely disappeared. All possible combinations 
 of these forms of pneumonia occur, and it has therefore seemed best 
 to consider all the cases in six groups into which they readily fall as 
 follows: (1) interstitial bronchopneumonia; (2) interstitial broncho- 
 pneumonia with lobular pneumonia; (3) lobular pneumonia; (4) lobar 
 pneumonia; (5) lobar with interstitial bronchopneumonia; (6) old 
 empyemas. • 
 
 It is, of course, possible that lobar and lobular pneumonia may occur 
 together, but I do not think that we have met with this combination. 
 
 Cases 14 to 58 were studied at Fort Sam Houston, Texas, Cases 
 165 to 205 at Camp Dodge, Iowa. 
 
 1 It has been pointed out by various writers that the term lobular pneumonia 
 should be applied to a consolidation involving a lobule, but such accurate limita- 
 tion does not take place. On the other hand, it is difficult to find any other 
 convenient term which will designate a patchy consolidation in which the alveoli 
 are filled with an inflammatory exudate of leucocytes and fibrin. Such an exu- 
 date is similar to that which when diffusely distributed over a whole lobe con- 
 stitutes a lobar consolidation, and it seems permissible to employ the term as a 
 conventional name for this condition. 
 
18 PNEUMONIA IN ARMY CAMPS 
 
 1. Interstitial Bronchopneumonia. 
 
 Case 14. — J. McL., age 22 yrs. Entered hospital Jan. 1, 1918, with typical 
 measles. Discharged Jan. 10. Second entry Jan. 16. Has not felt well since 
 leaving hospital, still coughs, has a fever and headaches. Diagnosis. — Acute 
 bronchitis until Jan. 22, when he became worse and was transferred to the pneu- 
 monia ward dehrious, very ill, and coughing. Signs of consolidation in right 
 lower lobe and rales over left lower lobe. Inspiration difficult. Marked cyanosis. 
 L"eucocytes 16,000. Temperature ranges from 99-104° F., pulse 100-150, respi- 
 ration 20-55. Died Feb. 2. Autopsy Feb. 2. 
 
 Anatomical Diagnosis: Bilateral interstitial bronchopneumonia with hemorrhage 
 aitd atelectasis; serofibrinous pleuritis (right). 
 
 Left pleural cavity. — There is no excess of fluid. Pleural surfaces smooth. 
 No adhesions. Right pleural cavity. — The cavity contains about 1,000 cc. of 
 slightly turbid brownish fluid with floating shreds of fibrin. Pleural surfaces 
 covered with thick, shaggy, yellow exudate of fibrin. Lymph glands in the 
 mediastinum enlarged. Left lung. — Surface is smooth. The lung is voluminous, 
 but the lower part of the upper lobe and the lower and posterior portions of the 
 lower are collapsed and pasty. Insufflation distends most of the upper lobe and 
 part of the lower. On section some of the bronchi of the upper lobe stand open 
 and are conspicuous as empty, thick walled grey tubes. They are surrounded 
 by areas of hemorrhage. In the lower lobe all the bronchi appear as thick 
 walled tubes with opaque yellow contents and are surrounded by hemorrhagic 
 areas which become confluent. In the larger bronchi the deeply congested 
 mucosa is covered by a thin opaque grey film. The bronchial glands are not 
 greatly enlarged. Right lung. — Greatly compressed by the pleural effusion. 
 It is covered by a layer of fibrin which varies from 2 mm. to 2 cm. in thick- 
 ness. The lymph glands at the hilum are greatly enlarged. All the lobes of 
 the lung are completely collapsed, but the upper lobe and the anterior portions 
 of the lower lobes may be distended by insufflation. In the lower and posterior 
 portions of the lower lobe there are numerous firm grey areas each of which 
 shows a central bronchus and a surrounding zone of hemorrhage. These foci 
 become confluent in places or stand out separately so that several may be seen in 
 each of the lobules of the lung. The lobules are sharply outlined by the inter- 
 lobular septa which are edematous and therefore conspicuous. 
 
 Cultures failed to grow through an accident. Smears from the lung showed 
 Gram-positive cocci in chains. 
 
 Microscopic Examination. — The left lung contains air and most of the alveoli 
 are unchanged, but many of the smaller bronchioles are filled with an exudate of 
 polymorphonuclear leucocytes among which a few streptococci are found. The 
 epithelium of such bronchioles is in places intact, in other places broken and 
 partly desquamated (Fig. 1). The wall is greatly thickened and its connective 
 tissue and smooth muscle elements are spread apart by red corpuscles and mono- 
 
WILLIAM G. MacCALLUM 19 
 
 nuclear wandering cells of various types. Wherever lymphatics are visible in 
 these walls they contain red corpuscles and mononuclear cells. The adjacent 
 alveoli are filled with blood, desquamated epithelial cells, and mononuclear wan- 
 dering cells together with a few polymorphonuclear leucocytes. The alveolar 
 walls are infiltrated with mononuclear cells and thickened. Both bronchi and 
 alveoli contain networks of fibrin. The alveoli which open directly into the 
 bronchi contain leucocytes in greatest abundance ; those which lie adjacent to the 
 wall of the affected bronchioles appear to contain blood and mononuclear cells 
 rather than leucocytes. Organization of the exudate in the bronchi is found in 
 an early stage in some places (Fig. 2). 
 
 The right lung shows a more advanced change. The pleura is covered with 
 fibrin upon the surface of which streptococci are found. The pleura itself is 
 densely infiltrated with blood. It is markedly thickened by the formation of a 
 vascular granulation tissue which has not destroyed all the remnant of the 
 pleural lining cells. The whole framework of the lung has become conspicuous 
 through the widening of the interlobular septa, peribronchial and perivascular 
 tissues, and the alveolar walls themselves by the most extensive infiltration of 
 mononuclear wandering cells. The lung is partly collapsed, but the enormously 
 thick walls of bronchi and alveoli are very distinct. It is especially in the neigh- 
 borhood of the infiltrated bronchi, interlobular septa, and pleura that the alveolar 
 walls are distended with cells. In the walls of blood vessels and bronchi and in 
 the interlobular septa lymphatics are easily seen. Most of them are thrombosed 
 and contain streptococci as well as lymphocytes and fibrin coagulum. The 
 more distant alveoli contain only masses of desquamated epitheUal cells. Those 
 nearer the bronchioles and participating in the formation of the peribronchial con- 
 soHdation are filled with dense fibrin together with the cellular elements described. 
 In this firm fibrin as well as in the bronchioles there is already visible a rather ex- 
 tensive growth of connective tissue. Definite strands of vascularized tissue are 
 seen in the lumen of some bronchi. In one there is a mass of such tissue covered 
 completely by a' continuous growth of bronchial epitheUum. The mediastinal 
 lymph glands are swollen, their marginal sinuses filled with large mononuclear 
 cells among which are many streptococci. These are entangled in a dense fibrin 
 network. 
 
 The other organs show nothing abnormal. 
 
 This is a typical case of interstitial bronchopneumonia following measles and 
 showing on one side empyema, collapse, peribronchial nodules with great inter- 
 stitial infiltration, thickening of pleura and septa, and advanced organization 
 of bronchial and intraalveolar exudate. 
 
 Case i5.— B. H., age 19 yrs. No history of measles. Since Jan. 3, 1918, cough 
 and expectoration with pain in chest and fever. Entered hospital Jan. 14. No 
 rash, no sore throat. Dulness and rales over whole right lung. Rales but no 
 duhi'ess over left. Leucocytes 16,800. Temperature 100-104° F., pulse 100-150, 
 respiration 30-60. Died Feb. 1. Autopsy Feb. 2. 
 
20 PNEUMONIA IN ARMY CAMPS 
 
 Anatomical Diagnosis: Bilateralinterslitial bronchopneumonia with fibrinopuru ■ 
 lent pleuritis. 
 
 Left pleural cavity. — Contains very little fluid. The surfaces are covered with 
 a thin exudate of fibrin which glues them together. Right pleural cavity. — 
 Contains about 1,500 cc. of turbid khaki-colored fluid with floating shreds of 
 fibrin. The lung is adherent in its upper posterior aspect; the lower lobe is 
 coUapsed and flattened. Left lung. — In both upper and lower lobes there are 
 collapsed areas, those in the lower lobe occupying the whole lower and posterior 
 portion. In the upper lobe there are a few bronchi filled with yellow plugs, 
 especially in the collapsed area. In the lower lobe these are much more nu- 
 merous and toward the hilum they are thickened and embedded in yellowish 
 opaque areas. There is no definite hemorrhage about them. The larger 
 bronchi are deeply congested. Right lung. — The pleura is thickened and 
 covered with a dense layer of yellow fibrin. The lung is completely collapsed 
 and flabby. It is studded throughout with yellowish areas of consolidated tissue 
 in the center of which there is generally to be seen the ragged lumen of a bronchus. 
 Such areas vary from 2 to 7 mm. in diameter, but in the lower lobe they become 
 confluent, in one place to form a mass 3 cm. in diameter. They are surrounded 
 by grey atelectatic lung substance. The bronchi are distinctly dilated toward 
 the periphery of the lung. Bronchial and peritracheal glands much enlarged. 
 
 Microscopic Examination. — The left lung shows the bronchioles throughout 
 their extent filled with a debris of epithelial cells, red corpuscles, and great 
 numbers of leucocytes among which streptococci are found in pairs and chains. 
 Gram-negative bacilH, apparently influenza bacilli, are also present. The epi- 
 thelium is greatly desquamated. The walls are thickened partly by the 
 great distension of the small blood vessels and the separation of the connective 
 tissue fibers, but chiefly by the infiltration of mononuclear cells. The lymphatics 
 are distended and contain mononuclear cells, red corpuscles, and streptococci. 
 The surrounding alveoli contain a few leucocytes, red corpuscles, desquamated 
 epitheKal cells, and fibrin. Mononuclear cells are also present. There is much 
 coagulated fluid in these alveoh. There are also a few areas in which the alveoli 
 are packed with polymorphonuclear leucocytes with little fibrin. In these areas 
 streptococci are found, although they are rare in the alveoH which contain mono- 
 nuclear and epithelial cells. 
 
 The right lung is much more extensively altered as though by a process of 
 longer standing. The pleura is converted into a thick granulation tissue with 
 blood vessels growing straight up into the hyaline fibrin. The bronchi are di- 
 lated, filled with leucocytes and disintegrated epitheUum. The epithelial lining 
 is largely destroyed and the walls are very greatly thickened and converted into 
 a sort of vascular granulation tissue densely infiltrated with mononjiclear cells. 
 For some distance round each bronchus the alveolar walls are greatly thickened 
 by the infiltrating mononuclear cells (Fig. 3). Elastic tissue stains show that the 
 framework of the alveolar wall is spread apart by these cells. The alveolar con- 
 
WILLIAM G. MacCALLUM 21 
 
 tents are composed of dense fibrin with desquamated epithelial and mononuclear 
 cells. Much of this exudate has undergone complete organization or replace- 
 ment by new vascular connective tissue which extends from the bronchi into 
 many alveoh. This gives added density to the consohdated areas. The walls 
 of the blood vessels are spread apart and thickened through the infiltration of 
 their adventitial coats. The interlobular septa are greatly widened by infil- 
 tration with fluid and cellular exudate and apparently also by the new formation 
 of connective tissue. However, lymphatics appear in the walls of the bronchi 
 and of the blood vessels and in these interlobular septa they are very wide and 
 filled with a coagulum of fibrin with blood corpuscles, leucocytes, and especially 
 mononuclear cells. These fibrin plugs are densely sown with streptococci which 
 are to be found there in enormous numbers even though search through the 
 lung tissue elsewhere fails to reveal them. This tends to support the view^that 
 they are in this way transmitted to the pleura. 
 
 Bacteriological cultures revealed Streptococcus hcemolyticus in the heart's blood 
 and lung. 
 
 This is a typical case of interstitial bronchopneumonia with empyema. There 
 is interstitial new formation and organization and streptococci show well in the 
 lymphatics. There is great thickening of alveolar walls and great density of the 
 exudate. In places there is lobular pneumonia. 
 
 Case. 16. — J. W., age 18 yrs. Entered hospital Jan. 24, 1918, with painful 
 cough which began 10 days previously. Had a chill 4 days ago. No history of 
 measles. On entry lungs showed dulness and rales in the right back, otherwise 
 clear. Leucocytes 22,200. Temperature 99-104° F., pulse 120-150, respiration 
 30-50. Died Feb. 2. Autopsy Feb. 2. 
 
 Anatomical Diagnosis: Bilateral interstitial bronchopneumonia with fibrinopuru- 
 lent pleuritis and pericarditis. 
 
 Left pleural cavity. — The lung is bound to the pleura by fresh fibrinous adhe- 
 sions. There is no fluid exudate. Right pleural cavity. — The surfaces are hemor- 
 rhagic and covered with a thick layer of fibrin which binds them together 
 anteriorly. In the posterior part of the cavity there is an accumulation of yellow 
 turbid fluid. Between the upper and lower lobes behind the midlobe there is an 
 enclosed pocket filled with this turbid exudate (Fig. 4). Pericardial cavity. — 
 Contains 500 cc. of turbid fluid. The surfaces are covered with a thick shaggy 
 layer of fibrin. Left lung. — The upper lobe is greatly distended with air and the 
 bronchioles are normal except in the lower part where they become the centers 
 of small grey nodules surrounded by hemorrhage. The lower lobe is completely 
 collapsed, and on section dark purple in color but studded with small grey nodules 
 about 2 mm. in diameter which in places become confluent. Right lung. — The 
 bronchial glands are much enlarged, the lung is very bulky and heavy and cov- 
 ered with thick fibrinopurulent exudate. Most of the lung except the apical 
 portion is collapsed. The smaller bronchi are grey and thickened, especially in 
 the lower lobe where they form innumerable small grey nodules, several to each 
 
22 PNEUMONIA IN ARMY CAMPS 
 
 lobule. The interlobular septa are prominent and grey. Liver. — Surface smooth 
 and mottled, lobules large and very distinct with grey margins and dark red 
 centers. 
 
 Microscopic Examination. — The right lung is most extensively affected, prac- 
 tically all the alveolar walls being much thickened by the mononuclear infiltration. 
 The changes in this lung are thus not exclusively in the bronchi. The pleura 
 is thickened by a vascular granulation tissue over which lies the fibrinous ex- 
 udate. This is best seen in the interlobar space where the fibrin loses its stain- 
 ing power where the bacteria become most abundant. Streptococci are present 
 in great numbers in certain rarefied areas and there many of them are enclosed in 
 phagocytes so that they look like little balls of organisms. The interlobular septa 
 are much thickened both by edema and new formation of connective tissue cells 
 and by infiltration of mononuclear cells. The lymphatics are often greatly dis- 
 tended and thrombosed and loaded with streptococci. The bronchi are filled 
 with leucocytes among which streptococci may be found. Many have lost their 
 epithelium. In others the bronchial epithelium is lifted up by a rich granulation 
 tissue which has developed beneath it. In all, the wall is greatly thickened and 
 very vascular and densely infiltrated with mononuclear cells. The alveoli in, the 
 neighborhood but also throughout rather wide areas of the lung substance contain 
 much free blood. This hemorrhage is widespread. They also contain dense 
 fibrin, desquamated epithelial cells, and mononuclear cells, but in many places this 
 type of exudate is replaced by newly formed connective tissue which is richly 
 vascular and which runs from one alveolus to another. In the alveoli which en- 
 close the denser masses of fibrin no bacteria are found. There are, however, a 
 few alveoli which contain polymorphonuclear leucocytes and these are fuU of 
 streptococci. In the bronchi the exudate is frequently replaced by long branching 
 cylinders of fresh vascular connective tissue. These may stretch from one wall 
 of the bronchus to the other (Fig. 5). The infiltration of the whole framework of 
 the lung with mononuclear cells and its general thickening through new formation 
 of connective tissue cells are a striking feature. 
 
 The bronchial lymph glands are swollen and hyperemic, their peripheral lymph 
 sinuses are full of large phagocytic cells, and often plugged by a fibrin network. 
 Bacteria are present, but not in great numbers and not in phagocytes. 
 
 The liver shows extensive fresh focal necroses mostly in a midzonal position. 
 They are irregular in form and extent. All the liver cells remain in position as 
 red necrotic cords, and leucocytes are packed among them. 
 
 The pericardium shows a rather fresh fibrinopurulent exudate without any 
 organization. The layer of lining cells is still intact. 
 
 Cultures from the heart's blood, lungs, and pericardial exudate showed Strep- 
 tococcus hcEmolyticus . 
 
 This is a typical case of interstitial bronchopneumonia with empyema and 
 pericarditis with exceptional infiltration and induration without very extensive 
 or marked peribronchial consolidation. Bacteria numerous in lymphatics. 
 
WILLIAM G. MacCALLUM < 23 
 
 Case 32. — R. S., age 25 yrs. Patient had a cold with cough dating from Dec. 
 15, 1917. Illness began with measles about Feb. 2, 1918; entered another 
 hospital Feb. 4. Transferred to this hospital Feb. 7. Still shows a fading macular 
 eruption and marked conjunctivitis. Throat injected and covered with whitish 
 membrane in patches. Dulness at the bases of both lungs behind. Breathing 
 not distinctly tubular. Rales over the whole lung. Temperature 99.6° F., pulse 
 120, respiration 32-34. Very restless and delirious. Died Feb. 9, 1918, 4.25 
 a.m. Sputum showed influenza bacilli and a few streptococci. Culture from 
 circulating blood gave no growth. Autopsy Feb. 9, 1918. 
 
 Anatomical Diagnosis: Clinical history of measles. Bilateral interstitial bron- 
 chopneumonia. Subacute fibrinous pleuritis. 
 
 Left pleural cavity. — The cavity contains a little yellowish fluid, about 150 cc. 
 At the apex of the lung are a few fibrous adhesions and denser ones exist between 
 the lower lobe and diaphragm. The pleura over the posterior surface of the lung 
 is dark greyish red and roughened by exudate. Right pleural cavity. — Largely ob- 
 literated by old adhesions especially in the lower part. There is no accumulation 
 of fluid and no fresh fibrinous exudate, but the surface is covered by a pleura 
 thickened to the consistency of stiff kid leather. Left lung. — The lung is volumi- 
 nous and in general distended with air except for one area of collapse in the lower 
 lobe. On section it is studded throughout with minute nodular areas of consoli- 
 dation which project like tubercles. The bronchi are somewhat reddened, the 
 bronchial glands moderately enlarged. Right lung. — This lung is insufflated with 
 air in all three lobes. The upper lobe shows some atelectatic patches which are 
 firmer than the remainder of the lobe. These are 2 cm. in diameter. On section 
 there are found scattered over the whole cut surface of the upper and lower lobes 
 small grey nodules 1 to 2 mm. in diameter which resemble miliary tubercles. On 
 close examination many of these nodules have a central depression which appears 
 to be the lumen of a bronchiole. Many of them are pale yellowish grey with a sur- 
 rounding paler grey zone. A few are surrounded by distinctly collapsed areas. 
 There are lobules in which a dozen or more of these nodules are visible on the cut 
 surface and in which hyperemia with some hemorrhage makes them stand out 
 prominently. In the more insufflated areas they are less conspicuous and it seems 
 possible that the thin grey halo may be due to collapse or obliteration of the im- 
 mediately adjacent alveoli. The bronchi are reddened but not dilated. 
 
 Epiglottis, uvula, larynx, and trachea show no especial abnormality, although 
 the lymph glands about the larynx are enlarged. 
 
 Microscopic Examination. — The pleural surface of the right lung shows a dense 
 vascular fibrous tissue beneath which is a looser tissue. There is a strand or two 
 of fibrin in its most superficial part. The interlobar space is obliterated by 
 similar tissue. 
 
 The bronchi are only slightly altered (Fig. 6). They are in their smaller 
 branches filled with leucocytes among which a few streptococci can be found. 
 No influenza bacilli can be found in the sections. The epithelium is irregularly 
 
24 PNEUMONIA IN ARMY CAMPS 
 
 interrupted, and in some cases extensively desquamated. In places leucocytes 
 have accumulated beneath it. The walls of these bronchi and bronchioles are in- 
 filtrated with cells among which there are a few leucocytes. Most of the cells, 
 however, are mononuclear wandering cells of the type of lymphocytes, a few 
 plasma cells, and cells of somewhat larger size with paler nucleus. The adjacent 
 alveolar walls are similarly distended and thickened with mononuclear cells. The 
 epithehum of the alveoli is partly desquamated. The alveoli contain leucocytes 
 in the areas round the terminations of the bronchi but there is very Kttle hem- 
 orrhage. Also there is very little fibrin and there are no soKd plugs such as are 
 seen in more advanced cases. There is, however, coagulated fluid which fills the 
 alveoli round the minute areas of consolidation. There are a few rather more 
 extensive patches of consolidation in which for some distance the alveoli are filled 
 with leucocytes, ragged networks of fibrin, blood, and coagulated fluid, but these 
 too are distinguished by the marked infiltration of the bronchial and alveolar walls 
 and the walls of the blood vessels with mononuclear cells (Fig. 7). Apart from 
 these the alveoli are filled with air and have thin, delicate walls until the pleura 
 or larger blood vessels are approached. There the thickening of the walls again 
 appears. The interlobular septa are not very conspicuous and microscopically 
 are not much infiltrated. Lymphatics can be injected from the pleura, and 
 although they contain some small plugs of fibrin and cells, the injection is fairly 
 complete. The mucosa of the trachea is much inflamed and infiltrated with 
 mononuclears. There are a few streptococci upon its surface. The tonsils show 
 many streptococci in their crypts. 
 
 Cultures from both lungs showed Streptococcus hamolytictis and the influenza 
 bacillus. 
 
 Case 34. — J. W. G., age 18 yrs. Said to have had measles at the age of 7. 
 Began to feel iU on Jan. 27, 1918, with coryza, conjunctivitis, sore throat, malaise, 
 and fever, but no chills. On Feb. 1 measles rash appeared and the patient en- 
 tered the hospital with a bad cough and abundant sputum. There was diffi- 
 culty in breathing, insomnia, and delirium. ■ Pharynx reddened, old Koplik 
 spots on buccal mucous membrane, dark purplish papular crescentic rash on face, 
 neck, chest, arms, and back. This later became confluent in places and assumed 
 a purpuric appearance. The rash began to fade on Feb. 5, but could he seen also 
 in the mouth. Breathing difficult especially on inspiration when accessory muscles 
 are brought into play. No definite localized dulness in the thorax nor any tubu- 
 lar breathing; moist rales heard everywhere. Feb. 6, (Dr. Cole) respiratory 
 movements slight, breathing almost entirely diaphragmatic. Marked retrac- 
 tion of lower chest on inspiration. Percussion note resonant over both sides 
 anteriorly and posteriorly. On auscultation, inspiration is loud and accompanied 
 everywhere by numerous coarse and medium mucous rales, but expiration is 
 practically not heard. Examination reveals no areas of definite impairment or 
 blowing breathing. Leucocytes 28,000. Temperature 100-104°F., pulse 100-140, 
 respiration 25-50. Died Feb. 10 at 2.30 a.m., 14 days after onset of measles. 
 Culture of sputum shows Streptococcus hccmolyticus . Autopsy Feb. 10. 
 
WILLIAM G. MacCALLTJM ' , 25 
 
 Anatomical Diagnosis'. Bilateral interstitial bronchopneumonia with fihrino- 
 purulent pleuritis. 
 
 Left pleural cavity. — Contains a moderate quantity of fluid which is turbid 
 and yellowish with a little floating fibrin. The pleura over the lung is dis- 
 tinctly thickened and white. Right pleural cavity. — Contains no excess of 
 fluid. The surfaces are smooth and glistening except over the posterior and 
 diaphragmatic surfaces where the gloss is lost. Left lung. — There are no adhe- 
 sions although the pleura is thickened and dull looking. The posterior and lower 
 part of the upper lobe is dense and on section it is found that in this region, which 
 extends about 4 cm. inward from the pleura, the interlobular septa are greatly 
 thickened and stand out prominently as greyish yellow ridges. The bronchi 
 are very much thickened and are filled with purulent exudate. In each of the 
 sharply outlined lobules there are several focal consolidations which correspond 
 with the terminal branches of the bronchi. The surrounding lung tissue is 
 greyish yellow, edematous, and rather translucent. The uppermost part of the 
 lung is air-containing (Figs. 8 and 9). Right lung. — The lung is voluminous and 
 its surface is smooth except over the base of the lower lobe where there is a thin 
 fibrinous exudate. In the upper lobe the interlobular septa are prominent and 
 there are a few projecting nodules which correspond to the bronchial branches. 
 The bronchi are very much thickened although the surrounding lung substance 
 appears to be air-containing. The lower part of the lower lobe shows the same 
 marking out of the lobules and thickening of the bronchi with small peribronchial 
 areas of consohdation. The upper portion and anterior parts of all the lobes are 
 air-containing. The bronchial glands are much enlarged. 
 Other organs appear normal. 
 
 Microscopic Examination. — The lungs show the most advanced changes. The 
 pleura over the left lung is thickened so as to form a layer of dense granulation 
 tissue upon the surface of which there is a thin interrupted layer of very compact 
 fibrin. The lymphatics in the pleura are not especially conspicuous. The inter- 
 lobular septa are very wide, as was observed in the gross specimen and are the 
 seat of a great quantity of fluid and a network of fibrin. There are streptococci 
 scattered in the meshes of this fibrin in small numbers. This edema and infil- 
 tration of the interlobular septa is not universal. In places the septa while 
 greatly thickened are quite dense and composed of new connective tissue. The 
 most striking feature of the sections is the presence of enormous lymphatics which 
 lie in the course of these interlobular septa or in one margin of the septum (Fig. 
 10). They form broad beaded canals often 2 mm. in width, each segment adjoin- 
 ing the next by a truncated end across which the septum can be seen. These 
 compress the adjacent alveoli. The endothehal lining can be seen clearly in 
 places. They are filled with leucocytes, fibrin, and coagulated fluid, and mingled 
 with these are enormous numbers of streptococci in rather long chains. 
 
 The bronchi are altered in extreme degree (Fig. 11). Few of them retain their 
 epithelial lining in anything like its normal arrangement. In some it is com- 
 
26 PNEUMONIA IN ARMY CAMPS 
 
 pletely desquamated, in others lifted up as a whole and collapsed together (Fig. 
 12). In still others it is stretched out so that the cells are much flattened. 
 Some of the bronchi show a high columnar epithelium which appears to form a 
 layer several cells deep. The lumen of the bronchus is filled with leucocytes or a 
 mixture of leucocytes, red corpuscles, and desquamated epithelium with many 
 streptococci, but no other organisms. The walls are greatly thickened and 
 extremely vascular. Many new vessels must have been formed, and there are 
 evidently many newly formed connective tissue cells. The wall is thus com- 
 posed of a loose vascular tissue which is densely infiltrated with mononuclear 
 cells of various types. None of these is ever very large, however. The same 
 is true of the alveolar walls in a decreasing degree as one passes from the 
 bronchus, large vessel, interlobular septa, or pleura into the lung substance. 
 Nevertheless there are many areas in which the alveolar walls are thickened 
 and infiltrated over a wide extent of tissue. In the alveoli near the affected 
 bronchi there are desquamated epitheUal cells and mononuclear wandering cells 
 together with a dense mass of fibrin. In many places this fibrin is distinct- 
 ly invaded by new connective tissue cells and in places even by blood ves- 
 sels. The organization is nowhere complete, however. The fibrin tends to 
 decrease as one passes from the bronchus, and the more outlying alveoli are 
 filled with fluid and red corpuscles. These together with the degenerated 
 and desquamated epithelial cells probably give the yellowish color to the 
 wide zones surrounding the affected bronchi. There are, however, in connec- 
 tion with some of these bronchi considerable areas of alveoli which are packed 
 with leucocytes held in a delicate network of fibrin and heavily loaded with 
 streptococci. The organisms in these patches are as numerous as one ever sees 
 pneumococci and are enclosed in phagocytes in the same way. That they are 
 streptococci is seen from their occurrence in long wavy chains, although most of 
 them are in pairs or short chains. The blood vessels are not markedly affected. 
 Thus in this case the advanced stages of the interstitial bronchopneumonia are 
 pretty well developed in association with patches of a more distinctly lobular 
 pneumonia, extensive collateral edema, and great distension of the lymphatics. 
 The enormous filling of the lymphatics with streptococci seems to afford the best 
 explanation of their transportation to the pleura. It is evident that the lymph 
 stream is stopped and that they must extend by their own growth. 
 
 The bronchial gland is densely infiltrated with large mononuclear cells so that 
 its architecture is almost obliterated. It is very hyperemic and contains enormous 
 numbers of streptococci in the sinuses. 
 
 Case 37. — A. H., age 24 yrs. Had pneumonia in 1914 when he underwent 
 an operation for resection of a rib for empyema. For several days prior to Jan. 
 28, 1918, had a cold. On that day felt sick, aching all over, chill with fever 
 and vomiting. Entered hospital Jan. 29. Examination Feb. 11 showed extreme 
 respiratory difficulty with cyanosis. Measles rash over whole body. Con- 
 junctivitis. Inspiration seems especially difficult and cyanosis is out of proportion 
 
WILLIAM G. MacCALLTJM 27 
 
 to the signs in th? chest. No definite duhiess or tubular breathing anywhere. 
 Large moist rales over the entire chest. Patient remained in same condition ex- 
 tremely sick until Feb. 13 when he died, 16 days after the onset of measles. Spu- 
 tum was yellow, mucopurulent, and contained influenza bacillus and Streptococcus 
 htBmolyticus. Blood culture taken Feb. 11 was negative. Autopsy Feb. 13, 
 1918, 1 hour after death. 
 
 Anatomical Diagnosis: Clinical history of measles. Bilateral interstitial broncho- 
 pneumonia with fibrinopurulent pleuritis. 
 
 Left pleural cavity. — Contains 500 cc. of turbid fluid with thick floating 
 shreds of fibrin; between the lung and the pericardium there are slight ad- 
 hesions. Right pleural cavity. — Obliterated by firm adhesions. There is a 
 scar in the posterior axillary line on the right side over the 9th rib, part of 
 which was removed in the old empyema operation. The two ends of the rib 
 are connected by fibrous tissue, and spicules of bone have grown out into 
 this portion which evidently contained periosteum. Left lung. — The lung is 
 not very voluminous, the lower lobe being partly collapsed. The upper lobe 
 is air-containing throughout, the apex and anterior border being especially 
 distended. At the upper posterior tip of the lower lobe there is a firm area. 
 Right lung {Fig. 13). — Voluminous and in general air-containing. There are, 
 however, some collapsed patches in which one can feel nodules. On section 
 the lung is found to be studded throughout with small greyish nodules which 
 project in groups of two or three. One can readily see with the naked eye that 
 they are the branches of the bronchioles with greatly thickened opaque yellowish 
 white walls and central lumen. Some of them are surrounded by zones of col- 
 lapse, others by a halo of dark greyish red. The bronchi when opened are grey, 
 not especially reddened or distended with exudate. The bronchial glands are 
 enlarged. Trachea and main bronchi are somewhat reddened. 
 
 Cultures at autopsy from the blood gave no growth. From the right lung 
 Streptococcus hamolyticus and the influenza bacillus were recovered. 
 
 Microscopic Examination. — The left lung shows a pleura slightly thickened and 
 composed of edematous new tissue covered with a dense layer of fibrin. The 
 bronchi are dilated and are quite large even near the pleura. The epithelium is 
 stretched out into thin flat cells. They contain leucocytes with very few strepto- 
 cocci in chains but great numbers of influenza bacilh. The walls of the 
 bronchi are extraordinarily thick. They are loose in texture as though spread 
 out by edema. The original tissue can no longer be recognized but is re- 
 placed by the lattice work of new fibers among which there are many mono- 
 nuclear wandering cells. The adjacent alveolar walls are distinctly widened by 
 the infiltration of such mononuclears, but they are not very thick. The alveoli 
 contain dense networks of fibrin, many desquamated epithelial cells, and some 
 mononuclears. In places there are alveoli filled with leucocytes. The inter- 
 lobular septa are not conspicuous, and lymphatics are hardly to be found. 
 The blood vessels are practically unchanged in appearance. Such a portion of 
 
28 PNEUMONIA IN ARMY CAMPS 
 
 the lung appears solid because of the confluence of the areas of consolidation 
 from one bronchiole to another. 
 
 In the right lung the striking feature is that the alveolar tissue between the 
 bronchi is air-containing and made up of very thin walled alveoli. The pleura is 
 thickened, but the thickening is produced by many frayed out layers of old fibrous 
 tissue which formerly bound the lung to the chest wall. There is no fibrin. The 
 interlobular septa are thick, dense, and fibrous without much evidence of recent 
 inflammatory change. The bronchi are greatly altered, and contain in most 
 cases a mass of leucocytes, but the epithelial lining is usually intact, at least 
 in part. The wall is very thick and dense and is somewhat infiltrated with 
 mononuclear cells. In many cases the great thickening of the bronchial wall is 
 all that attracts attention because the adjacent alveoli are normal. In other 
 places the epithelium is partly desquamated; the surrounding alveoli are filled 
 with organizing dense fibrin and mononuclear cells (Fig. 14). The organization 
 of the fibrin appears to begin in, or extend into the bronchi, for the exudate is 
 often found partly replaced by new connective tissue. There are in other places 
 still patches of alveoli directly associated with an affected bronchus which are 
 filled with leucocytes or fibrin. These give the character of lobular pneu- 
 monia, or would if they were extensive or numerous enough. 
 
 The dense old thickening of pleura, interlobular septa, and bronchial walls, 
 in contrast with the changes in the opposite lung, suggests that these more chronic 
 or finished changes may have dated from the time of his previous empyema with 
 operation. Nevertheless most of the small peribronchial foci of infiltration in 
 this lung which project like tubercles over the whole surface are undoubtedly 
 the result of the present infection. 
 
 Case 39. — C. L. A., age 19 yrs. Had whooping cough when a baby, measles at 
 the age of 9, diphtheria at 12, and mumps and scarlet fever at 14. Began on Jan. 
 23, 1918, with a chiU, fever, headache, and nosebleed. No conjunctivitis, coryza, 
 or sore throat. Has had no rash at any time, although on his transfer card was 
 the diagnosis measles. Entered hospital Jan. 25 with cough and shortness of 
 breath, with pain over left chest and left side of abdomen. Is extremely sick, 
 cyanotic, and cold. Breathing shallow and rapid. Clear mentally. Eyes 
 bright with no conjunctival hemorrhages. Physical examination of the chest 
 shows shifting flatness on the left side with tympany in the axilla and a definite 
 splash on shaking. Breath sounds over the tympanitic front are amphoric. On 
 the right side there is dulness over the lower back. Breath sounds distant; ex- 
 piration is indistinct. Numerous moist and sonorous rales. Heart is greatly 
 displaced to the right. On Feb. 13 aspiration of the left chest yielded a thin 
 purulent fluid which in films and cultures showed Streptococcus hcBmolyiicus in 
 pure culture. Sputum foul, greyish white, purulent, and tenacious. Contains 
 Streptococcus hcemolyticus and B. influenza;. Blood culture negative. Died 
 Feb. 14, 1918, 4 a.m. Autopsy Feb. 14, 1918, 10 a.m. 
 
WILLIAM G. MacCALLUM ' 29 
 
 Anatomical Diagnosis: Doubtful clinical history of measles. Bilateral interstitial 
 bronchopneumonia with fibrino purulent pleuritis and pneumothorax {left) . 
 
 Left pleural cavity. — Contains air. There are also 1,500 cc. of thin turbid 
 brownish fluid with very little floating fibrin. The sediment settles leaving the 
 fluid almost clear. Right pleural cavity. — Contains no excess of fluid. Pleural 
 surfaces anteriorly smooth and glistening, but over the posterior part of the lung 
 they have lost their gloss. Left lung. — The lung is small and heavy and appears 
 to be entirely collapsed. The pleura over it is grey, slightly thickened, and 
 studded here and there with hemorrhages over its sKghtly roughened surface. 
 The uppermost part of the upper lobe can be distended with air, but the lower 
 and posterior parts remain collapsed. The bronchi are dilated and thickened 
 and the small branches are surrounded by a grey-yeUow zone which is solid. 
 The upper part of the lower lobe can be distended. The lower part is soHd, 
 but it can be seen easily that each tiny branch of the bronchi is thickened and 
 surrounded by its own yellowish solid nodule and there it is the confluence of 
 these nodules which gives the soKdity to the whole. In the lowermost edge there 
 is even a portion which can be distended with air although most of the bronchioles 
 are packed with exudate. The bronchi are widened and their walls thickened 
 there also, and one has the sensation of cutting a rubber tube when they are 
 opened with scissors. Right lung {Fig. 15). — The lung is voluminous and shows 
 a smooth pleural surface. When distended with air it is found that a patch in the 
 upper lobe at the lower margin and one in the lower lobe above the middle re- 
 main dense and nodular. Each bronchiole on section is thickened and yellow 
 and surrounded with a little zone of consolidation and a wider zone of hemor- 
 rhage. The large bronchi are reddened, but the lung otherwise seems normal. 
 
 Cultures at autopsy from the pleural fluid, pericardial fluid, blood, and both 
 lungs show Streptococcus hcemolyticus . 
 
 Microscopic Examination. — The lesion in the left lung is rather more advanced 
 than in the right, but of the same character. The pleura is thickened, but inter- 
 lobular septa are not greatly widened. The bronchi in the left lung have in many 
 instances retained their epithehum, although the wall is greatly thickened and 
 infiltrated. Hemorrhage is common in this wall and in the adjoining tissue. The 
 infiltration and thickening of the alveolar walls extend quite wide of the bronchi. 
 In places there is complete loss of the epithelium, and a bronchus except for its 
 orderly arrangement of blood vessels in the wall would resemble an abscess. 
 Very few streptococci are visible even in the bronchi. The surrounding tissue is 
 consoHdated not only by the interstitial thickening of the alveolar walls, but by 
 the alveolar exudate which is composed partly of fibrin, blood, and epithelial cells, 
 and is partly already organized into a loose connective tissue. Hemorrhage is 
 abundant in the alveoli and in the tissues. There are several areas where the 
 alveoli are filled with an exudate of polymorphonuclear leucocytes. These are 
 somewhat richer in bacteria. 
 
30 • PNEUMONIA IN ARMY CAMPS 
 
 Case 41.— P. A. I., age 20 yrs. Began Jan. 28, 1918, with chill, fever, and 
 cough. Rash appeared Jan. 31, but there was no conjunctivitis or coryza. Ad- 
 mitted to hospital Feb. 2. Sweats profusely, complains of difficulty in breathing, 
 and coughs a great deal. There is marked cyanosis, patient half sitting up in bed 
 and bringing into play the accessory muscles of respiration. Face flushed, rash 
 well marked over the body. Pharynx very red. Dulness over left axilla and 
 lower back and in right interscapular region. Breathing distinct but not tubular. 
 Numerous sonorous rales. Left chest aspirated Feb. 13, but no fluid obtained. 
 Sputum grey and purulent and tenacious; contains Streptococcus hamolyticus as 
 predominating organism. Blood cultures made on Feb. 13 and 14 when patient 
 was dying gave pure culture of Streptococcus hcemolyticus . Died Feb. 14, 1918, 
 17 days after the onset of measles. Autopsy Feb. 14, 1918. 
 
 Anatomical Diagnosis: Clinical history of measles. Bilateral interstitial broncho- 
 pneumonia with serofibrinous pleuritis. 
 
 Left pleural cavity. — Contains about 300 cc. of turbid fluid with shreds of 
 fibrin. The pleural surface of the upper lobe of the lung is smooth, while that 
 over the posterior part and lower lobe is roughened by fibrin. Right pleural 
 cavity. — Contains about 500 cc. of turbid fluid. The surfaces are roughened by 
 fibrin. Left lung. — The bronchial lymph glands are very soft and large. The 
 bronchi contain a greyish mucoid material. The upper lobe of the lung is pale 
 and air-containing, the lower lobe partly airless and dark red. On section the 
 upper lobe is studded with small yellowish grey nodules 2 to 3 cm. in diameter 
 with a central lumen. These are prominent, but when the lung has been har- 
 dened and freshly cut they appear as small branching bronchi with thickened 
 walls and opaque purulent contents. In the lower lobe the bronchi are thick, 
 dark red, and prominent, and stand open. The nodules surrounding the small 
 ones are larger than in the upper lobe, granular, yellowish grey and red, and con- 
 fluent. Alveolar contents can be seen to project in these nodules. On longitu- 
 dinal section of the bronchi the yellow opaque contents contrast with the thick 
 grey wall and the outer zone of hemorrhages followed by the grey granular con- 
 solidation. The walls of these bronchi in the smaller branches are 1 mm. thick 
 (Fig. 16). Right lung. — The anterior portions of the lobes are air-containing, 
 while the posterior parts are dark red, heavy, and airless. The upper lobe can 
 be partly insufflated. It is studded with yellowish grey peribronchial nodules. 
 Interlobular septa broad and conspicuous. In the posterior part the lung be- 
 comes solid, the peribronchial nodules are large, 1 to 2 cm. in diameter, and 
 of a uniform yellow color (Fig. 1 7) . They have a ragged central bronchial lumen 
 and are separated from neighboring consolidations by a deeply hemorrhagic 
 solid lung substance. This contrast between bright yellow nodules of homo- 
 geneous consistency and the deep red intervening areas is very striking and gives 
 a peculiar marbling not seen in other cases. Nevertheless this is only an exag- 
 geration of the conditions found in other lungs. The lower lobe is firm and 
 densely studded with j-ather large peribronchial nodules about the smaller 
 
WILLIAM G. MacCALLUM 31 
 
 bronchi. It is the smaller branches of the bronchi whose walls become greatly 
 thickened. One finds on passing to the larger ones that their walls are practi- 
 cally unaffected. Bronchial glands are large and soft. 
 
 Cultures from the blood, lungs, and pericardial fluid showed Streptococcus 
 hcEtnolyticus in pure culture. 
 
 Microscopic Examination. — The same general condition is found throughout 
 both lungs. It is the interstitial bronchopneumonia described so often, but de- 
 veloped to its maximum. The pleura is not greatly thickened, but is covered 
 by a thin layer of dense fibrin in most places. The interlobular septa are wide 
 and contain large lymphatic channels choked and distended with masses of cells 
 and fibrin. Many of these cells are polymorphonuclear leucocytes, while others 
 are mononuclear cells. 
 
 The bronchi are dilated, often to such an extent as to reduce their lining epi- 
 thelium to a flattened layer throughout. It is probable that this is not a mere 
 effect of stretching, but is caused in part by this. The lumen is full of leucocytes 
 with relatively few streptococci. These organisms do not in this case penetrate 
 into the tissue in any great numbers and are scarcely to be found in the alveoli, 
 although they are found in the distended lymphatics. No other bacteria are 
 found. The wall of the bronchus is sometimes colossally thickened (Fig. 18) 
 and forms a dense mass of mononuclear wandering cells embedded in a meshwork 
 which is composed of the original connective tissue and muscle of the bronchus. 
 But to this there has evidently been added a great deal of new connective tissue 
 which is extremely vascular, especially just beneath the epithelium (Fig. 19). 
 Possibly this great vascularity represents only the extreme hyperemia of the pre- 
 existing tissue. One might regard this as the result of enormous hyperplasia of 
 the minimal supply of lymphoid tissue which exists in the normal bronchial 
 wall. Possibly that is a correct interpretation for some of it, since in other less 
 advanced cases it is sometimes seen that the lymphoid tissue is much increased 
 in bulk, and even becomes continuous to form a mantle about the bronchus. 
 Occasionally these bronchi are surrounded by air-containing tissue whose al- 
 veolar walls are then almost normal. But usually they are surrounded by a 
 considerable area of lung tissue consolidated by the filling of the alveoli with 
 blood, desquamated epithelial cells, and fibrin, together with a few mononuclear 
 cells (Fig. 20) . In such areas the alveolar walls are greatly thickened by mono- 
 nuclear invading cells, and this is especially true of the tissue about blood 
 vessels and septa. The appearance is similar to that seen in other cases except 
 that everything is exaggerated in this case. 
 
 The large dense yellowish white areas described in the upper lobe of the right 
 lung represent the extreme of this exaggeration. They have central bronchi and 
 are made up of tissue whose framework is densely infiltrated but whose alveoli 
 are filled with solid masses of fibrin enclosing very few cells. There are no leu- 
 cocytes and only a few remnants of epithelial or mononuclear cells. Blood has 
 ceased to exist in these alveoli, but there is a beginning organization of the fibrin. 
 
32 PNEUMONIA IN ARMY CAMPS 
 
 In the periphery of such areas red blood corpuscles become very numerous in the 
 alveoli and still farther out are the predominant elements. It gives the impres- 
 sion that red corpuscles were at one time present in the alveoli which are now so 
 densely filled with fibrin. The blood vessels in these lungs are not altered except 
 by the great infiltration of their walls with mononuclear cells, and in the larger 
 ones by the thrombosis of their adventitial lymphatics. They are never throm- 
 bosed. 
 
 Case 49. — C. P., age 21 yrs. No previous history of exanthematic disease. 
 On Feb. 9 vomited, after which he began to have fever. Next day noticed a 
 faint redness over the skin of the chest. Entered hospital Feb. 11 with a bright 
 red rash over chest, neck, face, abdomen, and arms. Diagnosis of scarlet fever 
 was made. Feb. 18, the urine showed a faint trace of albumin, no casts. Be- 
 came restless and delirious. Duhiess with rales over upper and midlobes of right 
 lung. Died Feb. 21, 1918. Autopsy Feb. 21, 1918, at 2 p.m. 
 
 Anatomical Diagnosis: Clinical history of scarlatina. Interstitial bronchopneu- 
 monia with empyema {right} . Bilateral lobular pneumonia. 
 
 Left pleural cavity. — Contains no excess of fluid. Surfaces of the pleura smooth 
 and glistening. Right pleural cavity. — The lower lobe of the right lung is adherent 
 by fibrinous adhesions to the costal pleura and diaphragm. The anterior margin 
 of the lung is adherent to the pericardium by light fibrinous adhesions. Between 
 the lower lobe and the pericardium there is a pocket containing about 75 cc. of 
 greenish yellow turbid fluid with shreds of fibrin. The upper lobe is coUapsed and 
 between it and the chest wall there is an accumulation of slightly turbid greenish 
 fluid in which there are large floating shreds of fibrin. The surface of all the lobes 
 is covered by a fibrinous exudate which in places measures 3 mm. in thickness. 
 Left lung. — The surface is smooth and the lung is in general air-containing and 
 easily inflated. In the anterior portion of the lower lobe there are several small 
 areas in which the alveoli are filled with an exudate of greyish red color. There 
 are also a few bronchi which show a thickened wall and are surrounded by a 
 hemorrhagic zone. Right lung. — The lung is small and collapsed with a thick- 
 ened pleura. The lobes are bound together and covered by a thick yellow coat of 
 fibrin. The upper lobe is air-containing in its apical portion but in the lower 
 part the bronchi are thickened and surrounded by greyish zones of consolidation 
 which tend to become confluent. The intervening lung substance is grey and 
 rather translucent. The lower lobe is uniformly studded in its posterior portion 
 with thickened bronchioles with grey confluent halos partly separated by a 
 darker grey-red intervening lung substance. The interlobular septa are wide 
 and prominent. The bronchial lymph glands are large and softened. Kidneys. 
 — No gross abnormality. 
 
 Cultures from pleural fluid, right lung, and heart's blood all show Streptococcus 
 hcemolyticus . 
 
 Microscopic Examination. — The right lung shows a thickened pleura with granu- 
 lation tissue covered with fibrin. The interlobular septa are wide and infiltrated 
 
WILLIAM G. MacCALLUM 33 
 
 with fluid, fibrin, and mononuclear cells. The lymphatics are not very con- 
 spicuous. The bronchi contain leucocytes and show desquamation of epithelium 
 with thickening, infiltration, and hyperemia of the wall. The adjacent and even 
 quite far distant alveoli present similar infiltration and thickening of their walls. 
 They contain much fluid with desquamated epithelial cells or are filled with dense 
 fibrin. Organization of this exudate has occurred in places. There are a few 
 areas in which the alveoli are filled with an exudate of leucocytes and fibrin, but 
 these are not so numerous as might be expected from the gross appearance. This 
 is essentially an interstitial bronchopneumonia following scarlatina, with very few 
 foci of lobular pneumonia. The sections show few streptococci but contain 
 large bacilli resembling B. siibtilis and many Gram-negative bacilli which appear 
 to be B. influenza. 
 
 Case 167. — W. J. H., age 27 yrs. Began with scarlet fever on Mar. 18, 1918, 
 and after recovery from that developed measles on Apr. 11. On Apr. 21 suffered 
 from severe pain in chest. Aspiration of the right pleura gave a turbid fluid 
 which contained Streptococcus hcemolyticus . The diagnosis of lobar pneumonia 
 with consohdation of the right lower lobe was made on Apr. 22, and confirmed 
 by x-ray. Empyema on the right side was recognized on May 1 , and the patient 
 died on May 4, at 6.15 p.m. Cultures at autopsy were contaminated, but the 
 blood showed Staphylococcus aureus, the left lung and right pleura a non-hemo- 
 lytic streptococcus. Autopsy May 5, 1918. 
 
 Anatomical Diagnosis: Interstitial bronchopneumonia with abscess formation. 
 Empyema {right). 
 
 There are two needle puncture wounds in" the midaxillary line on the right 
 side, one over the 6th, the other over the 7th interspace. Left pleural cavity. — 
 Contains no fluid. Surfaces smooth and glistening. Right pleural cavity. — 
 The anterior portions of the pleural cavity are free from adhesions and the 
 surfaces are smooth. Posteriorly there are adhesions which can be easily broken 
 through and there is then found behind the posterior part of the lower lobe 
 a cavity thickly lined with fibrinous exudate and containing about 50 cc. of 
 turbid brownish fluid. The lower part of the lower lobe is adherent. Left lung. — 
 Air-containing throughout except for a few obsolete tubercles. Right lung. — The 
 anterior portions of the upper and lower lobe and the whole of the middle lobe are 
 air-containing. The posterior part of the upper lobe is solid; the area of consoli- 
 dation measuring about 4 cm. in diameter is, on section, grey, smooth, and elas- 
 tic, with thickened pleura. Over the flabby, heavy posterior part of the lower 
 lobe there are large irregular areas where the pleura is smooth and glistening but 
 apparently necrotic. These areas are easily broken through, disclosing ragged 
 confluent cavities half filled with soft shreddy necrotic lung substance. On 
 section much of this lobe is collapsed without definite consolidation, but the 
 cavities are formed in a greyish red, smooth, and elastic area of consohdation. 
 They are crossed by bridges containing large blood vessels and are sharply out- 
 lined by a yellowish necrotic layer. A bronchus entering one of these cavities 
 loses its wall abruptly. 
 
34 PNEUMONIA IN ARMY CAMPS 
 
 Microscopic Examination.— The consolidated portion of the right lung shows a 
 great deal of thickening and infiltration of the alveolar walls, of the bronchi, 
 and of the interlobular septa. In places the interstitial thickening of the tissue 
 especially of the alveolar walls is great and there is much infiltration of poly- 
 morphonuclear leucocytes in addition to the mononuclear wandering ceUs. Many 
 of the alveoli are reduced to very small cavities lined with high cubical epithelium 
 or filled with desquamated epithelium. There is widespread organization of the 
 exudate. There are also some rather small patches of lobular pneumonia with 
 the alveoli filled with leucocytes. The cavities are formed, however, independ- 
 ently of these in the more indurated tissue in which there is chiefly desquamation 
 of epithelium. Their walls are made up of a layer of vascular granulation tissue 
 lined with necrotic material and fibrin. In other places there is no such granu- 
 lation tissue and merely the sudden cessation of the dense lung tissue and its 
 replacement by coagulated necrotic material. This is loaded with chains of 
 streptococci, but no other organisms are seen. 
 
 Case 171. — C. S., age 28 yrs. Had no predisposing disease. No history of 
 recent measles. Began suddenly on Apr. 21, 1918, with a pain in his chest. 
 The diagnosis of lobar pneumonia involving the right lower lobe was made upon 
 entrance into the hospital and confirmed by x-ray. The diagnosis of em- 
 pyema was made later and a resection for drainage was performed on Apr. 24. 
 The pleural fluid gave a culture of Streptococcus hcemolyticus . Died May 5, 1918. 
 Autopsy May 6, 1918. 
 
 Anatomical Diagnosis: Interstitial bronchopneumonia {right). Empyema (bilat- 
 eral). Acute nephritis. 
 
 Left pleural cavity. — Contains about 350 cc. of reddish brown liquid with 
 floating flakes of fibrin. The surfaces posteriorly are deep red in color and 
 covered with fresh shaggy fibrin. Right pleural cavity. — In the right back 
 
 4 cm. below the angle of the scapula and in the line of the 10th rib 
 there is a wound 6 cm. long which extends into the pleura. The right lung 
 is displaced far upward, the lower lobe being adherent behind between the 2nd 
 and 3rd. ribs. The apical part of the lung is densely adherent. The pleural 
 cavity extends about the back of the lung as high as the second rib and is widely 
 open below the lung. Its surfaces are covered with a thick yellow fibrinous exu- 
 date. Left lung. — The posterior portions of the upper lobe and most of the 
 lower lobe are collapsed but can be inflated easily. There are no areas of con- 
 solidation. The smaller bronchi are slightly reddened and contain sticky mucus 
 in the lower lobe but they are not thickened. Right lung. — The lung is com- 
 pletely airless except for a small part of the upper lobe. The lower part of the 
 upper lobe feels firm, the lower lobe flabby and soft. On section it is found that 
 the lower part of the upper lobe is uniformly consohdated through an area about 
 
 5 cm. in diameter. The middle lobe can be completely inflated. The lower lobe 
 presents in its posterior part some bronchi with purulent contents which are sur- 
 rounded by irregular grey patches of consolidation. The remainder of the lung 
 
WILLIAM G. MacCALLUM 35 
 
 is smooth and satiny on section but quite collapsed. Kidneys. — Alike and meas- 
 ure about 12 by 6 by 3.5 cm. They look rather swollen. The capsule strips off 
 smoothly leaving a greyish surface. On section the cortex measures 7 cm. in 
 thickness. It is pale and the labyrinthine portions of the striations are opaque 
 and yellow but straight. The glomeruli are visible as pale dots. 
 
 Cultures at autopsy from the right lung and both pleural cavities showed 
 Streptococcus hcemolyticus . 
 
 Microscopic Examination. — The consolidated portion of the upper lobe of the 
 right lung is found to be covered with a thick exudate of fibrin which overlies 
 a vascular granulation tissue. This tissue becomes very wide and edematous 
 at one point where it extends over the lung and connects with a broad inter- 
 lobular septum. Blood vessels are numerous in this tissue and the lymphatics 
 are wide but not thrombosed. The bronchi are very wide, their lining layer 
 thrown up into many folds. The epithelium is preserved and as a rule the lu- 
 men is filled with leucocytes among which are streptococci. The walls are mod- 
 erately thickened, hyperemic, and infiltrated with mononuclears. The lung 
 substance is in large part collapsed. The alveolar walls are not greatly infil- 
 trated or thickened but contain desquamated epithelial cells and fluid. There is 
 nowhere any exudate of leucocytes and nowhere much fibrin, although a little is 
 to be seen here and there. There are many alveoli in one part which contain 
 strands of a hyaline compact fibrin. In other sections the thickened bronchi are 
 conspicuous in a less atelectatic lung tissue. 
 
 The kidney shows in general a cloudy swelling of the epitheUum. The glom- 
 eruli are often rather enlarged and show capillaries distended with leucocytes 
 and blood, these elements being also found in the tubules. There is much inter- 
 stitial infiltration of the tissue with mononuclear cells and leucocytes in patches 
 which occur in both cortex and the outer zone of the pyramid. 
 
 In this case the lung is compressed by the pleural effusion, but itself shows rela- 
 tively little pneumonic alteration. Nevertheless there is a distinct infection of the 
 bronchi and a characteristic alteration of their walls. 
 
 Case 174. — G. R., age 28 yrs. No history of measles or other predisposing 
 disease. Began gradually on Apr. 5, 1918, with a pain in the chest and cough. 
 On Apr. 8 diagnosis of lobar pneumonia involving right lower lobe was made. 
 Radiograph on Apr. 12 showed involvement also of the right upper lobe with 
 possible accumulation of fluid in the pleural cavity. This was confirmed by 
 aspiration on the same day and the patient was referred to the surgeon for 
 operation. The 8th rib was resected and drainage established. Died May 7, 
 1918. Autopsy May 7, 1918, 5 hours after death. 
 
 Anatomical Diagnosis: Interstitial bronchopneumonia {right). Empyema with 
 operative drainage aiid multiple encapsulated residual collections of pus. Fresh 
 fibrinopurulent pleurisy {left) . 
 
 Left pleural cavity. — Contains about 1,500 cc. of opalescent yellow fluid, with 
 shreds of fibrin. The surface is covered with a very thick layer of loose shaggy 
 
36 PNEUMONIA IN ARMY CAMPS 
 
 fibrin which stretches across the cavity in great ropes. The lung is slightly 
 adherent at the apex and that portion is fairly voluminous. The rest of the 
 lung is plastered against the mesial surface of the cavity and is entirely col- 
 lapsed. The lower lobe is adherent to the diaphragm and to the posterior 
 wall of the pleura by fresh fibrinous adhesions. Right pleural cavity. — The upper 
 lobe of the lung is adherent by frail adhesions obliterating that part of the 
 pleural cavity. There are dense adhesions over the lower posterior border of 
 this lobe and the posterior part of the lower. There is a pocket of greenish 
 yellow pus between the pericardium and the mesial border of the middle lobe. 
 Over the 2nd and 3rd ribs there is a distinct pocket of pus which on removal of 
 the lung is left between two layers of the parietal pleura. Small pockets exist 
 between the base of the lung and the diaphragm. Lejt lung. — The lung is prac- 
 tically completely collapsed except at the apices of the lobes and is covered with a 
 thick fibrinous exudate. Inflation with air does not completely distend the whole 
 lung, leaving patches of collapse in the lower and posterior parts of both lobes. 
 There are some indefinite projecting greyish nodules in the posterior part of the 
 lower lobe, but otherwise there is no consolidation. Right lung. — The lung is 
 heavy. The anterior portions of all lobes appear to be air-containing. The 
 bronchial glands are large, dark greyish red, and pigmented. The surface of the 
 lung is torn by separation of old adhesions and cannot be inflated. On section 
 the upper lobe is normal in texture and air-containing. The lower lobe is also 
 air-containing except in the lower part which is pasty and airless and presents 
 some pale yellowish grey projecting nodules. The bronchi are not conspicuously 
 thickened in the rest of the lung. 
 
 Cultures at autopsy showed Streptococcus hcemolyticus in the heart's blood and 
 right and left pleura. Those from the lungs were sterile. 
 
 Microscopic Examination. — The left lung is fairly well distended. The pleura 
 is thickened and freshly vascularized and has lost its covering layer of cells. 
 The fibrin has been rubbed off in the section. The tissue itself shows no con- 
 spicuous interlobular septa, but all the bronchioles contain purulent exudate and 
 show infiltration of their walls which is sometimes quite marked. The alveoli 
 contain some fluid and some desquamated cells, but except in the neighborhood 
 of the bronchioles they are Httle altered. 
 
 The right lung is covered with a thick layer of granulation tissue with fibrin. 
 The interlobular septa are much more prominent than those of the left. The 
 bronchi in a section from the lower border of the lower lobe are all much infiltrated 
 with mononuclears and filled with purulent exudate. The alveolar walls are 
 greatly thickened everywhere and infiltrated with mononuclear cells, but they are 
 all collapsed and contain no exudate except a few desquamated epitheHal cells. 
 The lymphatics are in places filled with leucocytes, but are not prominent. This 
 appears to explain the gross appearance of such a lung which is soft and flabby 
 and rather satiny upon the cut surface. It is easy to recognize the fact that it is 
 collapsed and not filled with a fibrinous exudate, but the thickening of the alveolar 
 walls is likely to escape the unaided eye. 
 
WILLIAM G. MacCALLUM 37 
 
 Case 178.^-C. A., age 28 yrs. Began Apr. 22, 1918, with typical measles, 
 coryza, conjunctivitis, and red macular rash over body and face. On May 5, 
 began to have cough with sputum, and some dyspnea with cyanosis. There 
 was no definite dulness over the lungs, but riles could be heard everywhere. 
 ■ Voice became husky and at times was only a harsh whisper. By a great 
 efiort he could produce a tone. Sputum yellow, mucopurulent; loaded with 
 Gram-positive cocci which grew with slight hemolysis, thought to be staphylo- 
 coccus. Influenza bacillus also present. Blood cultures on May 7 and 9 nega- 
 tive. Died May 9, 1918, 4 days after the onset of the cough. Au*opsy 13 
 hours after death. May 10, 1918, 9 a.m. 
 
 Anatomical Diagnosis: Clinical history of measles. Interstitial bronchopneu- 
 monia {bilateral). Lobular pneumonia. Ulcerative laryngitis. 
 
 Left pleural cavity. — Contains no excess of fluid; surfaces are smooth and glisten- 
 ing. Right pleural cavity. — Contains no excess of fluid.. Surfaces are bright and 
 glistening throughout. There are no adhesions. The lungs are voluminous and 
 do not collapse. Left lung. — Readily inflated in all parts. On section it is air- 
 containing everywhere except for a few small areas in the upper lobe which stand 
 up above the surrounding lung tissue as greyish red elevated patches. In these 
 the alveoli appear to be filled with exudate. Throughout the remainder there 
 are small grey nodules which project slightly and are surrounded by hemorrhage. 
 These prove to be bronchi with purulent contents, thickened grey wall, and hemor- 
 rhagic halo. They become more numerous in the lower lobe and are especially 
 striking in the posterior part of the lung. Right lung {Fig. 21). — There are firm 
 nodules to be felt all through the lung. Some appear on section as greyish red 
 elevated patches with surface roughened by alveolar plugs. In the upper lobe 
 there are a few greyish nodules with central depression surrounded by a broad 
 hemorrhagic zone. These nodules which are much more numerous in the lower 
 lobe are traceable to the termination of the bronchi which upon being opened are 
 found to be filled with a purulent fluid. In the anterior portion of the upper lobe 
 and through the middle lobe these nodules are visible but appear to be in an even 
 fresher state and are represented by small bronchioles with slightly thickened 
 walls and no hemorrhages. Organs of the neck. — The whole pharynx, including 
 the base of the tongue, the tonsils, the posterior wall, and the pyriform sinuses, is 
 intensely reddened. The epiglottis is also bright red, but on its posterior sur- 
 face this color is mottled with small yellowish opaque areas with fairly smooth 
 surface. There are deep ulcerations of the vocal cords on each side (Fig. 22), 
 extending into the sinuses and on to the false vocal cords. 
 
 Cultures at autopsy gave Streptococcus hamolyticus from the heart's blood and 
 right lung. Streptococci were abundant in the fihn from the ulcer of the vocal 
 cords. Cultures from the spleen were sterile. 
 
 Microscopic Examination. — The lungs are about alike. The pleura is only 
 slightly altered in that it is hyperemic and sparsely infiltrated with mononuclear 
 cells. There is nothing left of the covering layer of cells, but no fibrin can be seen 
 
38 PNEUMONTA IN ARMY CAMPS 
 
 on the surface. The interlobular septa are very wide and large lymphatics can 
 be traced from the pleura into them. One or two of these show plainly by the 
 direction of their valves away from the pleura at a point about 2 mm. from the 
 pleural surface (Fig. 23) that the direction of the lymph stream is from the pleura 
 towards the hilum. They contain only fluid, but streptococci are to be found 
 in them in short chains and pairs. In places streptococci in numbers can be 
 traced into the substance of the pleura. The interlobular septa as they pass 
 deeper into the lung are edematous and contain a dense network of fibrin in 
 which are entangled many mononuclear cells. Two types of lesions are found 
 in the lung, one representing the acute lobular pneumonia, the other an early 
 stage of interstitial bronchopneumonia. There are only a few patches of the 
 former, while the latter is almost universal throughout the lung. Where the 
 lobular pneumonia occurs the changes in the bronchioles tend to be the same as 
 elsewhere, but are rather masked by the diffuse pneumonia. 
 
 These patches are fairly sharply outlined by small interlobular septa. They 
 show a uniform filling of the alveoli with an exudate composed of blood, fibrin, and 
 nucleated cells. Most of these cells are polymorphonuclear leucocytes, but 
 some are desquamated epithelial cells, while many are similar to lymphocytes 
 or are rather larger. The alveolar walls are not thickened as a rule, but in the 
 neighborhood of the interlobular septa they, like these septa, are infiltrated 
 with similar mononuclears. Streptococci are present in great numbers and ap- 
 pear in chains entangled in the fibrin, loose among the cells, or sometimes enclosed 
 in cells. They are especially numerous in the alveoli which border on the septa. 
 Where they lie amid red corpuscles, these have lost their hemoglobin and con- 
 trast sharply with those in the adjacent blood vessels. 
 
 In other parts of the lungs the lesions (Fig. 24) are concentrated about the 
 small bronchi leaving considerable intervening patches of air-containing tissue 
 with thin walled alveoU; the bronchioles are packed with a mass of cells and 
 streptococci. The bacteria are ranged along the walls in clumps and strands. 
 The cells in this exudate are much fragmented and distorted and it is difficult to 
 determine their nature, but it is certain that while many of them are polymorpho- 
 nuclear leucocytes nearly as many are mononuclear wandering cells. They are 
 held in a network of fibrin. The epithehum of the bronchi is lost and they are 
 Kned by a thin layer of coagulated necrotic material. The wall is edematous and 
 spread out and densely infiltrated with mononuclear cells. The blood vessels 
 are distended, but the process is fresh and the wall does not look hke granulation 
 tissue with radially arranged blood vessels, as is the case in some instances in 
 which the disease has been of long duration. The lymphatics in the outer part 
 of the bronchial wall are wide and closely packed with leucocytes, mononuclear 
 cells, and bacteria. The adjacent and continuous alveoli have walls which are 
 slightly thickened by mononuclear infiltration. They are filled with dense fibrin 
 containing distorted cells, some of which are polymorphonuclear, while many 
 can be recognized as mononuclear cells. Red blood cells are frequent in these, 
 
WILLIAM G. MacCALLXJM 39 
 
 and in the more distant alveoli are present in great quantities. Practically no 
 bacteria are found in the exudate in these alveoli. The blood vessels are not 
 especially changed.- The bronchial glands are large, the lymph cords very wide 
 and evidently containing many new cells. But the sinuses are especially widened 
 and packed with mononuclear cells and leucocytes. They contain great quanti- 
 ties of streptococci often scattered diffusely but quite often in dense clumps. 
 Streptococci are strewn along the surface of the mucosa of the trachea and are 
 undoubtedly present in enormous numbers in the ulcerations of the vocal cords 
 and other parts of the larynx. This specimen has not been cut for microscopic 
 study. 
 
 Case 184.-— 'i. B., age 22 yrs. Negro. On Apr. 29, 1918, had measles. On 
 May 2 he was found to present the physical signs of lobar pneumonia with con- 
 solidation of the left lower lobe, dulness, bronchial breathing with a few large 
 riles. Sputum bloody. Sputum on May 8 was mucopurulent and nummular, 
 containing Gram-positive cocci. Cultures showed Streptococcus hcemolyticus and 
 Staphylococcus aureus. Blood culture was negative on May 7. Temperature 
 high at the beginning, 104-105°, later reduced to 101°. Leucocytes 9,000. Died 
 May 10, 1918, at 9.45 p.m. Autopsy 38 hours after death. The body had been 
 embalmed so that cultures failed to grow. 
 
 Anatomical Diagnosis: Interstitial bronchopneumonia (bilateral) with dissemi- 
 nated lobular pneumonia. Ulcerative laryngitis. 
 
 Left pleural cavity. — Contains about 10 cc. of fluid. The surfaces are clear and 
 smooth. Right pleural cavity. — Contains no fluid. The surfaces are smooth. Left 
 lung. — The lung is blue and heavy in the posterior portion, but both lobes are air- 
 containing anteriorly. Upon artificial insufflation both lobes are pretty well dis- 
 tended but firm nodules can be felt which on section project above the cut surface 
 (Fig. 25). They are grey, rough, and granular, and when cut in certain directions 
 show a central lumen. In the lower part of the lung they are almost confluent 
 and are embedded in deeply hemorrhagic collapsed patches. The bronchi are 
 deeply reddened and dilated in their peripheral parts where they are filled with a 
 bloody purulent exudate. The nodular consolidations which lie about their ter- 
 minal portions are much more numerous and more nearly confluent in the posterior 
 part of the lung. The bronchial glands are enlarged, greyish red, and firm. 
 Right lung. — The lung is smooth superficially, but there are a few hemorrhages in 
 the pleura between the lobes. The lower lobe is heavy and nodules can be felt 
 throughout it. The middle lobe is collapsed posteriorly but inflated anteriorly. 
 The upper lobe is more air-containing but also feels nodular. In the upper lobe 
 on section it is found that the bronchi are thickened, reddened, and dilated at 
 their ends. They are accompanied or surrounded by elevated consolidated areas 
 which are ragged in outline and rough and spongy. The bronchial walls are 
 opaque and lined with a dull grey material. The finer bronchioles still appear 
 as lumina in the centers of consolidated areas which are surrounded by hemor- 
 rhagic zones. Such lesions are found in the posterior part of the middle lobe and 
 
40 PNEUMONIA IN ARMY CAMPS 
 
 more abundantly in the lower lobe where they tend to become confluent. Pharynx 
 and larynx {Fig. 26). — The tonsils are not especially enlarged. The pharyngeal 
 wall is reddened and the left side of the epiglottis and left arytenoepiglottic fold 
 and adjacent tissues are edematous. There is definite ulceration of the vocal 
 cords and there are other ulcerations below them which extend on the walls of the 
 larynx. There are quite deep ulcerations at the base of the epiglottis. The 
 tracheal mucosa is much reddened. 
 
 Microscopic Examination. — The lung shows a combination of the lesions of in- 
 terstitial bronchopneumonia and lobular pneumonia. The pleura is not thickened 
 and shows no evidence of fibrin on its surfaces. The interlobular septa are quite 
 inconspicuous and none of them shows any special edema or infiltration, or 
 even the distension of the lymphatics. 
 
 The bronchi on the contrary are wide and very conspicuous (Fig. 27). Each 
 branch is surrounded by a denser lung tissue, but there are some other patches 
 of consolidation which extend away from the bronchi. There is a ragged mass 
 of debris in the lumen of each. This contains many red corpuscles, polymorpho- 
 nuclear leucocytes, as well as fragments of necrotic cells. Streptococci in tangled 
 masses are ranged along the walls of the bronchi, but there are no influenza 
 bacilli. The epithelium is entirely destroyed and in its place there is a rather 
 thick layer of coagulated necrotic tissue. Outside this in the larger bronchial 
 branches there are remains of mucus glands, etc. In general the wall has assumed 
 the character of a loose edematous granulation tissue with abundant wide blood 
 vessels arranged more or less radially and a profuse infiltration with mononuclear 
 wandering cells of various sizes. If this granulation tissue is in any way derived 
 from the swelling and spreading apart of the lymphoid tissue in the wall of the 
 bronchus, which has occurred to me as a possibility, it must at least have under- 
 gone an extraordinary change. Lymphoid tissue can be seen at certain points, 
 but it does not form in this case as in some others a complete mantle about the 
 bronchi, and most of the bronchial wall seems actually to be composed of granu- 
 lation tissue. The lymphatics in the outer layer of the wall are' wide and gen- 
 erally filled with a clot which entangles red corpuscles, mononuclear cells, and 
 chains of streptococci. The adjacent lung tissue is consohdated by the filUng 
 of the alveoli with dense fibrin in which there are to be found a few desquamated 
 epithehal cells and mononuclear wandering cells. It is striking that the epitheHal 
 cells when not desquamated are much more nearly cubical than normal, and 
 among these plump cells one may find mitotic figures (Fig. 28). The alveolar 
 walls are thickened also and are infiltrated with mononuclear cells. This is not 
 extreme, however, and a much more remarkable infiltration of this sort is found 
 in the walls of small vessels in such a neighborhood. 
 
 The other areas of consohdation mentioned above as not so intimately related 
 to the bronchial thickening are patches in which the interstitial changes are 
 slightly developed but in which all the alveoli are filled with dense masses of 
 polymorphonuclear leucocytes in a delicate network of fibrin or alone (Fig. 29). 
 
WILLIAM G. MacCALLXJM , 41 
 
 Among these there are enormous numbers of streptococci, although there are 
 none in the denser plugs found in the alveoli about the bronchi. These areas 
 fade at the margin into patches of edema. There are quite extensive areas in 
 which the thin walled alveoli are distended with fluid without any cells and in 
 these alveoli too, chains of streptococci are found. 
 
 Case 191. — S. F., age 22 yrs. Negrb. No history of previous illness. No 
 record of measles. Began suddenly on Apr. 13, 1918, with pain in chest and chill. 
 Diagnosis of lobar pneumonia involving left lower lobe was made, and later, on 
 May 5, there was found also a lobar consolidation of the right lower lobe. The 
 existence of empyema on the right side was recognized by aspiration on May 13. 
 A yellow serum with greenish white sediment loaded with streptococci in short 
 chains was removed. These proved to be Streptococcus hamolyticus. Blood cul- 
 tures on May 11 were negative. Died May 14 at 5.30 p.m. Autopsy May 15, 
 1918. 
 
 Anatomical Diagnosis: Interstitial bronchopneumonia {left lower and right upper 
 and lower lobes) . Disseminated lobular pneumonia. Empyema {right) . 
 
 Left pleural cavity. — Contains no excess of fluid. There are a few fresh adhe- 
 sions over the lower edge of the upper lobe. The surface of the pleura is dull. 
 Right pleural cavity. — Contains about 700 cc. of thick greenish yellow pus which is 
 distributed in the space between the lung and the pericardial sac, in the meshes of 
 adhesions between the lung and diaphragm, and about the apex of the lung. 
 There are easily torn adhesions over the back of the lung which seem to separate 
 into spaces which are filled with purulent fluid. Pericardium. — Contains no ex- 
 cess of fluid and the lining surfaces are smooth, but there are bright petechial 
 hemorrhages over the posterior surface of the heart with shreds of fibrinous ma- 
 terial overlying them. Left lung {Fig. 30). — The posterior surface is roughened 
 by fibrin especially over the lower lobe and between the lobes. The upper and 
 anterior part of the upper lobe is air-containing, but the posterior and lower part 
 is firmer. On section, although this lobe is easily inflated, there are found in the 
 lower portion numerous firm projecting nodules surrounded by hemorrhagic zones. 
 The lower lobe contains only a little air-holding lung tissue and is not inflated by 
 attempts to blow air into it. On section it is found to be thickly studded almost 
 everywhere, but especially in the lower part, with nodules which are surrounded 
 by hemorrhage and show a central depression which corresponds with the lumen of 
 the bronchiole. The bronchial glands are enlarged and greyish red. Right lung. — 
 The surface and the interlobar spaces are occupied by fibrin as described. The 
 whole lung is collapsed and flabby except for a small portion of the anterior half 
 of the upper lobe. Even after inflation the lower portion of this lobe is collapsed 
 and shows numerous bronchi with thickened walls which appear as definite 
 nodules. In the lower lobe collapse is extensive and there are many greyish 
 nodules which surround the lumina of bronchi. There is also some patchy con- 
 solidation of a deep greyish red color rather different in appearance from the 
 nodules. Pharynx and larynx.— There is slight reddening throughout, but no 
 
42 PNEUMOIOA IN ARMY CAMPS 
 
 ulceration of the vocal cords although there is a discoloration as though from a 
 healed ulceration just below the cords. 
 
 Cultures at autopsy gave Streptococcus hcemolyticus in pure culture in the 
 heart's blood, right and left lung, right pleiu-a, and pericardium. 
 
 Microscopic Examination. — The right lung shows a thick pleura composed of 
 highly vascularized granulation tissue covered with fibrin. There are strepto- 
 cocci on the surface of the fibrin. The interlobular septa are not much widened 
 but the lymphatics are sUghtly distended with clots which contain leucocytes and 
 fibrin. 
 
 The bronchi are full of half necrotic leucocytes with abundant streptococci and 
 influenza bacilli. The epitheUum is largely desquamated and the walls are con- 
 verted into a vascular granulation tissue which is much infiltrated with mono- 
 nuclear cells, evidently derived in part from a thickening of the lymphoid tissue 
 of the wall. 
 
 The alveolar walls are not thickened or infiltrated. The alveoli are mostly 
 collapsed, their walls very hyperemic. Those near the bronchi are free of blood 
 and their walls are sometimes infiltrated with red corpuscles. Many of the 
 nearby alveoK are partly filled with desquamated epithelial cells, but there is also 
 a great deal of fluid. Some contain dense plugs of fibrin which have undergone 
 little or no organization. Hemorrhage is widespread about these bronchioles. 
 
 In many places the bronchi are surrounded by patches of lung tissue in which 
 the alveoli are filled with leucocytes whose polymorphous nucleus is plain. These 
 are often studded with streptococci. Indeed in some places the alveolar walls 
 have become necrotic. Some of these areas of lobular pneumonia are extensive 
 and no doubt necrosis of the tissue occurs commonly in the larger ones. 
 
 Case 193. — A. M. M., age 23 yrs. Began suddenly without previous iUness or 
 history of measles on May 3, 1918, with chUl and fever. On May 5 the diagnosis 
 of lobar pneumonia was made with involvement of the left upper lobe. Sputum 
 on May 8 was tenacious and mucoid without blood, and contained Gram-positive 
 diplococci which proved to be Pneumococcus Type III. Staphylococcus aureus 
 was also present. Blood culture on May 8 showed a few non-hemolytic strep- 
 tococci. Another on May 9 was negative. Died May 16, 1918, at 8.15 a.m. 
 Autopsy May 17, 1918, 21 hours after death. 
 
 Anatomical Diagnosis: Old interstitial bronchopneumonia with abscess formation 
 (left upper lobe). Fibrinous pleuritis. Hyaline degeneration of rectus abdominis 
 muscle. 
 
 Left pleural cavity. — Contains no fluid. The surfaces are smooth except that 
 the posterior part of the upper lobe is adherent to the costal pleura by easily 
 broken adhesions, and the base of the lung to the diaphragm by old adhe- 
 sions. Right pleural cavity. — The cavity is almost entirely obliterated by old 
 adhesions which are especially dense between lung and pericardial sac, and 
 between the base of the lung and the diaphragm. Left lung. — The lung is volumi- 
 nous and in the upper lobe there can be felt a sohd mass occupying the upper 
 
WILLIAM G. MacCALLUM 43 
 
 posterior part. The pleura has lost its gloss over the solid part but is smooth 
 over the anterior part which is air-containing. On section the consolidation is 
 fairly uniform, pale greyish red, and presents a rather rough surface which is 
 distinctly translucent. The lower part is perhaps slightly redder than the 
 upper. About the middle of this lobe there is a large abscess cavity reaching 
 practically to the pleura but not perforating it. This cavity measures 5 cm. in 
 diameter, is of extremely irregular outline with lateral excavations, and com- 
 municates widely with the large bronchus which opens abruptly into it. It con- 
 tains a yellowish purulent exudate and there is a shreddy dark greenish grey 
 necrotic tissue hanging from the wall. The wall is made up of a thin line of 
 opaque yellowish material. In the anterior part of the upper lobe the inter- 
 lobular septa are quite distinct. In places there are small grey projecting nodules 
 related to the bronchi. The lower lobe is air-containing throughout. The 
 bronchial glands are large, pale, and greyish, and studded with pigment. The 
 large bronchi contain a thick frothy mucopurulent exudate. Right lung. — The 
 lung is torn in removal and roughened by old adhesions, but it is air-containing 
 throughout and of normal texture. The bronchial glands are not enlarged. 
 Pharynx and larynx. — Normal. 
 
 Cultures taken at autopsy showed Streptococcus hamolyticus in the heart's 
 blood and left lung. 
 
 Microscopic Examination. — The tissues of the upper lobe of the left lung show 
 most advanced changes. The pleura is thickened and dense and is covered 
 with a thin layer of fibrin. The interlobular septa and the whole connective 
 tissue framework of the lung are enormously thickened and condensed. There 
 has evidently been a great new formation of connective tissue, for this widening 
 is not due to edema but to the formation of closely knit fibrous tissue. The lym- 
 phatics are wide and in places contain some free cells, but most of them are 
 partly or completely obstructed by masses of vascularized connective tissue which 
 have evidently resulted from the organization of thrombi formed in the lym- 
 phatics at an earlier stage. The bronchi are filled with purulent exudate which 
 contains large numbers of streptococci. The epithelium is in general preserved, 
 but the walls are greatly thickened both by new formation of connective tissue 
 and a dense infiltration of mononuclear cells. Lymphatics in their walls are in 
 places obliterated by newly formed connective tissue. The alveolar walls are 
 thickened everywhere, partly by infiltration of wandering cells but partly by 
 newly formed connective tissue. They are in most places filled with a mass of 
 desquamated epithelium, some mononuclear cells and leucocytes, and fluid. Fibrin 
 is not so conspicuous as usual, but perhaps chiefly because most of it is replaced 
 by strands of connective tissue which fill the alveoli in places. The epithelium 
 when it is preserved is high and cubical. Red blood corpuscles are abundant 
 in places so that the alveoli are full of blood. The most striking feature, therefore, 
 is the advanced interstitial infiltration and induration together with the organi- 
 zation of the exudate both in the alveoli and lymphatics. One section passes 
 
44 PNEUMONIA IN ARMY CAMPS 
 
 through the abscess which is filled with polymorphonuclear leucocytes with bac- 
 teria. The lining layer of the cavity is densely infiltrated with large vacuolated 
 cells. Outside this layer the lung tissue for some distance is much indurated 
 and every alveolus is filled with a solid plug of connective tissue. Organization 
 has evidently proceeded rapidly here. Sections through other parts of the lung 
 show it to be air-containing, but the septa and perivascular and peribronchial 
 tissues are greatly thickened and some alveoli are filled with desquamated cells 
 and wandering cells. Lymphatics in the septa in this part of the lung (lower 
 left lobe) contain abundant leucocytes and fibrin. 
 
 The rectus abdominis muscle which appeared normal to the unaided eye 
 shows most extensive hyaline degeneration and disintegration of the muscle 
 fibers which are broken into formless clumps. These are surrounded by nuclei 
 many of which are undoubtedly the nuclei of the sarcolemma. These some- 
 times appear to coalesce into giant cells. But there is also a definite reaction 
 on the part of the interstitial tissue and blood vessels and numerous mono- 
 nuclear phagocytes are present. 
 
 In attempting to present these diseased conditions according to 
 their etiological agents, if we group the cases of pneumonia which 
 are caused by the hemolytic streptococcus in several classes so as 
 to emphasize one or the other of the predominant lesions, it is only 
 to facilitate the description of that lesion, as one might describe sepa- 
 rately tuberculous pneumonia and miliary tuberculosis of the lung. 
 The combination of the streptococcal lesions is almost as common 
 as the occurrence of several types of tuberculous lesion in the 
 same lung. In the group of cases just described the attempt has 
 been made to select those which show in its purest form the so called 
 interstitial bronchopneumonia, but even so some trace of lobular 
 pneumonia can be found in all but a few. Nevertheless, in whatever 
 combination they occur, even when associated in the same lung 
 with the lobar pneumonia caused by the pneumococcus the character- 
 istics of the interstitial bronchopneumonia stand out distinctly. 
 
 The typical change in the pleura consists in the effusion of a large 
 quantity of thin turbid fluid into the pleural cavity. This is usually 
 brownish with a fine granular sediment which is stirred up on moving 
 the lung, but there are generally also floating shreds of fibrin. The 
 surface of the pleural membranes is covered with fibrin under which 
 hemorrhages are often visible. It is remarkable, however, that 
 thickening of the pleura by the formation of new granulation tissue 
 
WILLIAM G. MacCALLUM 45 
 
 takes place very rapidly. This is a common condition, but there are 
 cases, especially those in which adhesions had existed, in which there 
 is no exudation, and others of recent origin in which although the 
 lungs are diffusely affected the pleural surfaces are perfectly smooth 
 and the cavity is practically dry. There are various later modifi- 
 cations of the character and distribution of the effusion leading to 
 its encapsulation and to a more definitely purulent character which 
 forms the rule in cases which survive long enough. In view of the 
 interest devoted by surgeons to the question of empyema, an analysis 
 of the condition in all the cases in this series will be given later in 
 this paper. 
 
 The gross appearance of the lungs in the cases of interstitial broncho- 
 pneumonia varies with the age of the lesion. The powers of resistance 
 of the individual doubtless have much to do with this also, and it 
 seems that in those with little resistance the type of lesion is different 
 and tends to the lobular form. At first it seemed merely a surmise 
 that the lesions confined to the bronchioles and their immediate en- 
 vironment were early changes, since some cases, such as No. 14, 
 showed these very slight alterations in one lung in a patient in whom 
 the other lung was in an advanced stage. Nevertheless, the occur- 
 rence of death after 7, 4, 8, and 7 days of pulmonary involvement in 
 Cases 32, 178, 184, and 194 has shown that what appeared to be fresh 
 lesions really do occur in the cases of briefest course. The early 
 lesions in the opposite lung in older cases must simply represent 
 fresh lesions in a case in which elsewhere similar changes have long 
 been developed. 
 
 The lung may be collapsed, since that is largely an effect of the pres- 
 sure of a large pleural effusion, or, as in Case 32, both lungs may be 
 distended with air.^ In such a case as No. 32 the lesions appear as 
 minute projecting nodules often grouped in twos and threes, several 
 being found within the area of a lobule. In Cases 14 and 194 these 
 small lesions show the branching of the terminal bronchioles and are 
 
 2 When the lung is inflated artificially with air it is easy to see the lesions 
 which are submerged in the general blue-grey of the collapsed area. For that 
 reason we have frequently blown up these lungs with a bulb tied into the bron- 
 chus spreading open the collapsed alveoli and aerating the blood in their capil- 
 laries so that it becomes bright red. Then the actual lesions become very distinct. 
 
46 , PNEUMONIA IN ARMY CAMPS 
 
 rendered conspicuous by their halo of hemorrhage. In Case 178 this 
 became very brilhant since each bronchus could be traced often in 
 complete longitudinal section by the grey thick wall, its yellow 
 contents, and its envelope of hemorrhage. 
 
 In Case 37, which was of 16 days duration, there was no extensive 
 peribronchial consolidation, but the bronchi were so greatly thickened 
 as to project in firm tubercle-like nodules. 
 
 In Cases 29 and 34, of 20 and 14 days duration, the lesions expand 
 from the bronchi into patches of firm yellowish consolidation 3 to 5 
 mm. in diameter which project as nodules on the cut surface. 
 The intervening lung substance in such cases, aside from the hemor- 
 rhage spread around these peribronchial nodules, is greyish, elastic, 
 and edematous, while the interlobular septa are thickened, yellow or 
 white, and opaque, and stand up like low stone walls which separate 
 fields. They divide the cut surface into startlingly distinct lobules 
 and in each of these there are several nodules. In Case 41 there are 
 the most advanced lesions, although the course of the disease was only 
 17 days. Not only are the bronchi enormously thickened, but the 
 peribronchial nodules of consolidation are larger than in any other case 
 and stand out as firm dense and perfectly homogeneous yellow elevated 
 patches, each with its central bronchiole and its halo of hemorrhage. 
 In one or two of the cases of long duration, Nos. 167 and 181, which 
 lasted 23 and 46 days, and in one of the fresher cases. No. 193, which 
 lasted only 14 days, we found abscesses with actual cavity formation, 
 the contents of the necrotic areas being discharged through the bron- 
 chi. This is a frequent occurrence in the cases of lobular pneumonia 
 and remains to be described in other cases, but it is not so frequent in 
 those in which the lesion takes the form of the interstitial broncho- 
 pneumonia. The essential features, therefore, in the gross appearance 
 of the lungs in interstitial bronchopneumonia lie in the filling of the 
 bronchioles with opaque exudate, the thickening of their walls, and 
 the consolidation of the adjacent lung tissue which appears in cross- 
 section as a nodule, in longitudinal section as a branching mantle 
 of dense tissue bordered with hemorrhage accompanying the bron- 
 chiole. Atelectasis of the intervening lung substance, great thick- 
 ening and prominence of the interlobular septa and pleura, and 
 usually pleurisy with abundant effusion make up the whole picture. 
 
WILLIAM G. MacCALLUM 47 
 
 The bronchial glands are somewhat enlarged and soft. The mucosa 
 of the large bronchi is deeply reddened and covered with purulent 
 exudate, sometimes with a necrotic pseudomembrane. Some writers 
 have insisted that this should be called purulent bronchitis or bron- 
 chiolitis, but the involvement of the whole lung takes place so 
 promptly, including the framework and the pleura, that I think the 
 term bronchopneumonia is better justified. 
 
 The microscopic study of the early changes shows essentially an in- 
 fection of the bronchi with streptococci. The greatest stress should 
 be laid upon the staining of bacteria in the tissues because it is only 
 in that way and not by mere report of the presence of cultivable 
 streptococci that we may determine the exact topographical relation 
 of these organisms or others to the lesion.^ It is found that in every 
 
 ^ A new stain which is a combination of Goodpasture's and the Weigert fibrin 
 stain has served well to demonstrate in the tissues Gram-negative organisms, 
 such as the influenza bacillus, in red and Gram-positive bacteria in blue. Dur- 
 ing the correction of the proof of this paper the cases have been restudied with this 
 stain. It is as follows: 
 
 1. Stain for 10 minutes to i hour or more in Goodpasture's stain, which is: 
 
 cc, 
 
 30 per cent alcohol 100.0 
 
 Basic fuchsin . 59 
 
 Aniline oil 1.0 , 
 
 Phenol crystals 1.0 . 
 
 2. Wash in water. 
 
 3. Difierentiate in 40 per cent formaldehyde solution (pure formalin). This 
 requires only a few seconds. The bright red color washes away and gives place 
 to a clear rose color. 
 
 4. Wash in water. 
 
 5. Counterstain in saturated aqueous picric acid. The section should re- 
 main until it assumes a purplish yellow color, about 3 to S minutes or less. i 
 
 6. Wash in water. 
 
 7. Differentiate in 95 per cent alcohol. The red color reappears and some of ' 
 it is washed out. Some of the yellow of the picric acid is also washed out. 
 
 8. Wash in water. 
 
 9. Stain in Stirling's gentian violet 5 minutes or more. , 
 
 10. Wash in water. 
 
 11. Gram's iodine solution. 
 
 12. Blot dry without washing. 
 
 13. Aniline oil and xylol (equal parts) until no more color comes away. 
 
48 PNEUMONIA IN ARMY CAMPS 
 
 instance the streptococci are present in numbers among the leuco- 
 cytes which fill the bronchioles. They can be traced along the mucosa 
 of the larger bronchi up into the trachea where possibly other bacteria 
 may also be found, but in the terminal bronchioles there are in 
 many instances only streptococci. In some cases there are relatively 
 few, while in others, such as Nos. 184 and 178, they are present in 
 tangled masses strewn along the mucosa but in smaller numbers in 
 the center of the bronchial lumen. Recent papers from England 
 and France, already referred to, declare for the preponderant part 
 played by the influenza bacillus. A glance at the table given above 
 will show that it has been found quite commonly in the sputum in 
 these cases too, sometimes in the lung and pleural fluid. Its relation 
 to these lesions must be left in some doubt since it is present in 
 only part of the cases while the streptococcus is invariably present. 
 The British writers describe a purulent bronchitis or broncho- 
 pneumonia which resembles this most closely and regard it as due 
 to the influenza bacillus, although they frequently found an associ- 
 ated Streptococcus pneumonic^ (pneiunococcus) and Streptococcus 
 longus* 
 
 The epithelium of the bronchus is usually intact, but in some cases, 
 Nos. 178 and 184, it is quite destroyed and even the underlying tissue 
 is necrotic for a considerable depth. This appears to the naked eye 
 as an opaque greyish yellow pseudomembrane lining the bronchus 
 down to the finest ramification and extending out to the largest 
 branches. In the earliest stages, as in Case 32, the respiratory 
 bronchioles are the ones affected, while the larger bronchi show little 
 
 14. Two changes of xylol. 
 
 15. Balsam. 
 
 Gram-negative organisms are red. Gram-positive blue. 
 
 Dr. Goodpasture's own method is not yet published but he kindly allows me 
 to use his formula in describing this method. Goodpasture's stain corresponds 
 with the first seven maneuvers given above. 
 
 ^ During the epidemic of influenza which raged through September and Octo- 
 ber, 1918, we have encountered cases in which the influenza bacillus occurred in 
 pure culture in the lungs and bronchi. In these the lesions resembled very 
 closely those which are described here under the name interstitial broncho- 
 pneumonia. (Note made during the correction of the proof.) 
 
WILLIAM G. MacCALLUM 49 
 
 change. Leucocytes with streptococci extend out into the lateral 
 vestibules and into the terminal ones and even into the ultimate al- 
 veoli. There is little other change, but although the more distant 
 alveoli are not altered, the bronchial wall and the adjacent alveolar 
 walls even at this stage are infiltrated with wandering cells. There 
 are few of them at this stage, but they give a distinct character which 
 comes out clearly in later stages. 
 
 In all the later stages this change in the connective tissue, elastic 
 tissue, and musculature which make up the wall of the bronchus is 
 striking. The normal elements are spread apart by great numbers of 
 mononuclear cells which intercalate themselves between the fibers 
 and often form a mass which lifts up and dislodges the epithehum. 
 Most of these cells are small like lymphoid cells, but many are larger, 
 occasionally assuming the character of plasma cells or the various 
 types of larger mononuclear wandering cells. Edema accompanies 
 them and aids in the spreading apart of the connective tissue. The 
 blood vessels are distended with blood and evidently new ones are 
 formed with associated fibroblasts, for in many cases the wall assumes 
 the appearance of a highly vascular granulation tissue in which the 
 blood vessels come to be radially placed. In some cases the bronchi 
 become dilated, occasionally to a marked degree, as in Case 181, and 
 to a less extent in Cases 41 and 184. In the most advanced conditions, 
 as in Case 41, the walls of the bronchioles become enormously thick- 
 ened and form a compact tube of infiltrated tissue, but in most in- 
 stances the wall is rather relaxed and loose in texture. With dila- 
 tation the epithelium may be stretched and flattened or it may dis- 
 appear by being desquamated, leaving the surface of the new granula- 
 tion tissue exposed. 
 
 The normal wall of the smaller bronchi contains only a relatively 
 small amount of lymphoid tissue, scattered in thin strands in its outer 
 layers, except at certain places such as the points of division where 
 somewhat more compact masses often occur. About the same may be 
 said of the adventitia of the blood vessels and the interlobular septa. 
 It seems possible, however, that much of the infiltration which has 
 been described, and a part of the thickening of the bronchial wall may 
 be due to the swelling and spread of the lymphoid tissue all along the 
 wall of the bronchus, and its appearance of being a new growth of 
 
50 PNEUMONIA IN ARMY CAMPS 
 
 granulation tissue with radially arranged and abundant blood ves- 
 sels may well be explained in the same way, since with a greatly 
 thickened mantle of lymphoid tissue there would arise a more con- 
 spicuous vascular supply for that tissue. 
 
 The lymphatics which run in the bronchial wall are distended with 
 leucocytes, mononuclear cells, and blood, and usually thrombosed 
 with great quantities of streptococci entangled in the thrombus. 
 Before discussing other parts of the lymphatic network, however, we 
 must describe the alveolar structure of the lung. 
 
 It has been said that in the earliest stages the alveoli about the 
 terminal bronchioles contain leucocytes and streptococci. That 
 seems to be a transient condition, however, for in stages only a little 
 older a different condition is found. Even in the early lesions in 
 Case 14, in which the opposite lung showed old lesions, the bron- 
 chiole is distinctly infiltrated and thickened, and the affection extends 
 through the wall to the adjacent alveoli. These are filled with blood, 
 the lining epithelium is beginning to desquamate, and there are some 
 mononuclear cells. 
 
 In the later stages a uniform process appears which is a combina- 
 tion of these. The alveolar walls contiguous to the bronchi become 
 widened and thickened by an invasion of mononuclear cells just as ^ 
 in the bronchial wall itself. The alveoli are partly filled with fluid 
 and with desquamated alveolar epithelium. Many of them a little 
 farther removed are quite filled with red corpuscles and all con- 
 tain dense masses of compact fibrin in which cells are partly entangled. 
 Mononuclear cells escape into the alveoli, but in small numbers. It is 
 strange that although streptococci are found in the lumen of the 
 bronchus among the polymorphonuclear cells which persist there, and 
 in still greater numbers in the thrombosed lymphatics of the wall, 
 they are not to be found in these distended alveoli, which seems to 
 show that this process has a certain protective influence. 
 
 A later stage, as in Cases 29, 15, 16, 34, or best of all 41, shows the 
 wide extension of this process of filling up the alveoli with dense 
 fibrin in solid but rather contracted plugs which occupy only part 
 of the space, epithelial cells, fluid, and blood. The fluid which ex- 
 tends far wide of the actual area of consolidation is evidently very 
 thick and viscous, for it coagulates in fixation into a brittle mass 
 
WILLIAM G. MacCALLUM 51 
 
 which takes a deep stain. The infiltration of the alveolar walls 
 sometimes produces a great thickening. The cells accumulate on 
 each side of the centrally placed layer of capillaries and lift away 
 from them the delicate structureless membrane which on each side 
 forms the wall of the alveolus upon which the epithehal cells are laid. 
 This is very distinct in spite of the text-book statement that there is 
 but one structureless membrane in each alveolar wall. This infiltra- 
 tion is most marked in the immediate neighborhood of the bron- 
 chiole, in the neighborhood of blood vessels whose adventitial walls 
 are thickened in the same way, and again in the neighborhood of the 
 pleura and the interlobular septa. In other parts of the lobule the 
 alveolar walls maintain their proper thickness for a long time and in 
 many cases are air-containing and normal in appearance where they 
 lie apart from the foci of consolidation. Where the alveolar walls 
 are rendered dense and not easily stretched, the alveolar epithelium 
 becomes thick and cubical ; frequently one may find mitotic figures in 
 these cells, indicating plainly their active multipUcation which must 
 be necessary to produce such numbers as are found shed into the cavi- 
 ties of the alveoli. It is astounding to find that even before the 
 later stages just described have been reached, organization of the 
 exudate has begun. In the bronchioles of the tiny hemorrhagic foci 
 in Case 14, and in the alveoli and bronchi of many of the other cases, 
 new blood vessels are found to have grown into the exudate carrying 
 fibroblasts and replacing the fibrin with vascular connective tissue. 
 The origin of this from the walls of the bronchioles and its ex- 
 tension into many alveoli is often seen. Connective tissue may spring 
 up through a defect in the epithelium of the bronchial wall and 
 stretch across the lumen to connect with the opposite wall or it may 
 form a column which reaches down into the alveoli and forms a sort 
 of mold of the original air spaces. Epithelium grows over it rap- 
 idly and whole fields may show the alveoli fairly occupied by strands 
 of pretty dense connective tissue, suppHed with blood vessels and 
 clothed in epithelium. 
 
 The blood vessels of the lung are not especially altered. I have 
 found none thrombosed, and the circulation is unimpaired. The 
 circulation is indirectly embarrassed in two ways by the same means. 
 The obstruction of the bronchi by infected material need not extend 
 
52 ' PNEUMONIA IN ARMY CAMPS 
 
 into the alveoli of its own respiratory district, although the inflam- 
 matory process extends through the wall to the neighboring alveoli, 
 but it does prevent the entrance of air. The atelectasis which re- 
 sults from this is rendered general and complete by the pressure 
 exerted on the lung by an effusion of fluid into the pleura, and the 
 lung as it appears when removed from the body is commonly a flabby 
 pasty soft grey-blue mass which has been plastered against the verte- 
 bral column and compressed into an airless substance. The blue 
 color at once indicates its filling with venous blood, for when it is dis- 
 tended it quickly becomes bright red. This must be due to the 
 angular kinking of the venules which prevents the proper egress of the 
 blood. This is supported by the fact that in old cases of empyema in 
 which the condition has lasted a long time the alveoli are filled with 
 epithelial cells loaded with iron pigment which are so characteristic 
 of chronic passive congestion. One may conclude that there is a 
 chronic passive congestion, caused by local pressure which indicates 
 that the passage of blood is impeded and necessarily the whole circu- 
 lation in some degree obstructed. 
 
 The pleural changes have been mentioned. The pleura itself is 
 sometimes smooth, sometimes covered with a thin film of fibrin, but 
 most often with a thick shaggy layer of fibrin into which it throws up 
 blood vessels and connective tissue, by this process converting itself 
 into a thick layer of granulation tissue. This is, of course, continued 
 into the pleural surfaces of the interlobar spaces where, however, it 
 is limited by the ready formation of adhesions. 
 
 The interlobular septa which run downward into the lung from the 
 pleura have become especially interesting in this disease because of 
 their own changes and because of the lymphatics which run in their 
 substance. The septa themselves become edematous and their con- 
 nective tissue fibers are spread wide apart. A coagulum of fibrin in 
 which there are entangled numerous mononuclear wandering cells 
 forms in the fluid in the meshes of this tissue. At a later stage this 
 condition which renders the septa very conspicuous, as in Cases 34 
 and 29 and others, gives place through abundant formation of new 
 connective tissue to one in which the widened septa are found to be 
 composed of dense fibrous tissue, as in Cases 35, 193, 57, 58, and 
 others. 
 
WILLIAM G. MacCALLTJM 53 
 
 The lymphatics of the lung have been the object of much study 
 (Miller, Cunningham, and others), but even yet there is not per- 
 fect unanimity of opinion about their arrangement and more 
 especially about the course of the stream of lymph. According to 
 Miller's description, they run in the septa and in the walls of the 
 blood vessels and bronchi toward the hilum of the lung where they 
 empty into the sinuses of the bronchial glands. On the pleural 
 surface, or rather in the substance of the pleural membrane, lymphatic 
 channels which form a dense network are connected with those in the 
 substance of the lungs. Miller states that the current from the super- 
 ficial layers of the lung is directed away from the hilum and toward the 
 pleural network and that this is supported by the direction of the 
 valves toward that network. I have made some injections in dis- 
 tended lungs after having first filled the blood vessels with carmine 
 gelatin. The lymphatics were injected with Berlin blue through a 
 fine hypodermic needle inserted into the substance of the pleural 
 membrane. A most extensive and complete injection of this network 
 can be seen to shoot out over the surface of the lung and from it larger 
 trunks dipping into the substance of the lung suddenly appear as they 
 are filled with the blue mass. A fairly complete injection of the peri- 
 vascular and peribronchial and septal lymphatics as far as the hilum 
 of the lung can be made in this way, showing the latter channels to be 
 very wide. It seems probable from experience with the injecting of 
 lymphatics elsewhere that no such complete injection could be made 
 with moderate pressure if many valves had to be forced backward. 
 Further a fortunate section or two showing the lymphatics of the 
 interlobular septa in direct connection with those of the pleural net- 
 work reveals the fact that the undisturbed valves actually open away 
 from the pleura even at a distance of only a few millimeters from the 
 surface. This is shown in Fig. 23. I think, therefore, that in the 
 lymphatic apparatus of the lung the natural current is from the 
 pleural surface toward the hilum of the lung. 
 
 In all the cases of interstitial bronchopneumonia, the lymphatics 
 as seen in section, whether in the walls of the bronchi and blood 
 vessels, in and about the interlobular septa, or in the pleura, become 
 conspicuously dilated and are frequently filled with a thrombus. 
 These thrombi are entirely analogous to thrombi which might form 
 
54 PNEUMONIA IN ARMY CAMPS 
 
 in veins except that they contain no red corpuscles and are not con- 
 structed on the pecuHar framework of platelets which appear so regu- 
 larly in the venous thrombi. Platelets, of course, must be practically 
 absent from the fluid lymph in such peripheral lymphatics so that the 
 materials for the construction of an elaborately formed thrombus are 
 lacking. The lymphatic thrombi are mere formless coagula of fibril- 
 lated fibrin in which leucocytes and many streptococci are entangled. 
 They must effectively obstruct the channel when they are large 
 enough and thus divert the current into other paths. 
 
 In many cases the lymphatics distended in this way with opaque 
 yellowish pus or clots loaded with leucocytes become most conspicu- 
 ous on the cut surface of the lung. They are sometimes 2 to 3 mm. 
 in width and distinctly beaded as they run along the course of the 
 interlobular septum. Many of them can be traced to their connection 
 with the pleural network which may be similarly distended with a 
 yellowish white mass. On section, as shown in Fig. 10 from Case 
 34, they appear as huge varicosities in the course of the interlobular 
 septum and are filled to distension with leucocytes and streptococci. 
 In one lung which was shown me they were so large as to be mistaken 
 for bronchi. 
 
 It seems that this constant infection of the peribronchial and other 
 lymphatics in the early stages of the disease, with a real concentra- 
 tion of bacteria in the lymphatics, must play a part in the early pro- 
 duction of pleural infection. Of course the idea of transportation of 
 the bacteria by the lymph to the pleura is opposed by the state- 
 ment made above that the current is all in the opposite direction, but 
 with the entrance of the bacteria the lymphatics become obstructed 
 and the current stops. Direct extension by growth is visible in these 
 lymphatics in sections, and that seems to afford the most plausible 
 explanation of the early infection of the pleura. Other arguments 
 concerning pleurisy may be more satisfactorily discussed later in 
 connection with empyema. 
 
 These then are the main points in the anatomy of the interstitial 
 bronchopneumonia in as far as the lung is concerned. It appears as a 
 primary infection of the bronchioles. In the course of the affection 
 thickening and infiltration of the bronchial and alveolar walls, of the 
 interlobular septa, perivascular adventitial tissue, and of the pleura 
 
WILLIAM G. MacCALLUM 55 
 
 occur. The lymphatics are widely infected and thrombosed. The 
 alveoli about the infected bronchi are filled with fluid and blood, dense 
 coagula of fibrin appear, the epithelial cells multiply and are shed 
 into the lumen, a few mononuclear cells appear, and organization 
 takes place in this exudate until bronchi and alveoli contain strands 
 of fibrous tissue. In the meanwhile the infection probably extending 
 by growth along the lymphatics reaches the pleura and sets up a 
 pleurisy with effusion, one effect of which is to cause extensive col- 
 lapse of the lung. It is important to consider at this point the dis- 
 tribution of the bacteria in the lung in this affection. The exudate 
 in the lumen of each bronchiole always contains streptococci in con- 
 siderable numbers; the lymphatics in the bronchial wall and those 
 seen elsewhere contain them in numbers in the thrombi; the superficial 
 layers of the exudate on the pleural surface contain a perfect feltwork 
 of these organisms sometimes enclosed in leucocytes; but the contents 
 of the alveoli and the substance of the tissue contain none. Even 
 in the bronchial wall it is generally impossible to trace the bacteria 
 into the crevices of the tissue. In the pleural exudate it is the super- 
 ficial layers which contain them ; the fluid exudate is a thick suspension 
 of bacteria, but they are found in rapidly decreasing numbers as one 
 passes into the substance of the fibrinous exudate, and in the pleural 
 granulation tissue there are none. Since they find the conditions for 
 their life so unsuitable in the depths of a fibrinous exudate there must 
 be rapid additions to those in the lymphatics to maintain their num- 
 bers. It is interesting to observe their behavior upon the surface of 
 the lobulated mediastinal fat which hangs in the pleural cavity 
 near the apex of the heart. Wherever the surface was exposed the 
 streptococci were numerous ; where two folds had adhered so that the 
 crevice between them was obliterated by a fibrinous adhesion the bac- 
 teria descended to the depth of the open crevice, but there were none 
 in the deeper obliterated part, nor anywhere in that tissue. 
 
 All this must signify a definite power of resistance on the part of the 
 tissues in these cases, indicating their ability to destroy the organisms 
 whenever they come into sufficiently close contact with the living 
 cells, for as we shall see in the next two groups of cases a different 
 lesion is developed in those patients, apparently because they have 
 little of this power of resistance. While streptococci are present in 
 
56 PNEUMONIA IN ARMY CAMPS 
 
 relatively small number in the interstitial form, in which bulwarks 
 are built up against them, they swarm in direct contact with the 
 tissues in the lobular pneumonia and cause extensive necrosis. The 
 contrast between their distribution in interstitial bronchopneu- 
 monia and that of pneumococci in lobar pneumonia is also striking 
 because the pneumococci are scattered evenly throughout the depths 
 of a pleural exudate and everywhere in the contents of the alveoli. 
 
 Small foci of lobular pneumonia occur in many of these cases, 
 but the next group is set apart as illustrating more fully this com- 
 bination. 
 
 2. Interstitial Bronchopneumonia and Lobular Pneumonia. 
 
 Case 24. — A. G. C, age 25 yrs. Measles and mumps in childhood. Taken sick 
 Jan. 15, 1918, with sudden pain in the right side. Next morning fever and ex- 
 treme weakness. Entered hospital Jan. 16. Dulness over right lung in front 
 with tubular breathing and rales. Left lung hyperresonant. Leucocytes 18,800. 
 Temperature 98-105° F., pulse 94-155, respiration 20-55. Died Feb. 4. Au- 
 topsy Feb. 5, at 5 p.m. 
 
 Anatomical Diagnosis: Interstitial bronchopneumonia with disseminated lobular 
 pneumonia. 
 
 Left pleural cavity . — Contains no fluid; surfaces are dull and hyperemic over 
 the posterior portion of the lung. Right pleural cavity. — Contains no fluid. 
 There are light fibrous adhesions easily broken through over the posterior 
 portion, and the surfaces are injected. Heart. — The pericardial cavity con- 
 tains a few cc. of fluid; its surfaces are glistening. The heart is of moderate 
 size, flabby, and soft. The endocardium of the right side is smooth, tricuspid, 
 and the pulmonary valves are delicate. The mitral valve is thickened and 
 shortened but not definitely stenosed. The chordse tendineae are also involved 
 in this thickening, but the mitral ring measures 8.5 cm. in circumference. On the 
 anterior leaflet there are several massed vegetations which form a clump about 1 
 cm. in height. These are rough and crumbly. There is a smaller vegetation at 
 the middle of the leaflet while the large mass extends somewhat on the posterior 
 leaflet. The aortic valves are delicate and competent. The coronary arteries are 
 smooth. In the myocardium of the septum beneath the endocardium is a small 
 pale fleck surrounded by hemorrhage. Left kidney. — Contains an anemic infarc- 
 tion about 1 cm. in diameter. Lejt lung. — Voluminous. The upper lobe is 
 easily and completely insufflated, the lower lobe less so, leaving superficial collapsed 
 areas. On section the upper lobe is air-containing throughout. Lower lobe is 
 spongy and apparently largely air-containing. There are coalescent grey spongy 
 patches surrounding blood vessels or bronchi which are separated especially near , 
 the surface of the lung by deep red areas. There are no definite nodules nor 
 
WILLIAM G. MacCALLUM 57 
 
 even any definite consolidation. No distinct thickening of bronchial or blood 
 vessel walls is to be observed and there is no pleurisy. Right lung. — Edematous 
 and densely studded with greyish nodules of consolidation which are conspicu- 
 ous on a dark red background. 
 
 Microscopic Examination. — The lung shows no change in the pleura. There is 
 but slight thickening of the interlobular septa. The bronchi are filled with an 
 exudate of leucocytes. The walls are somewhat thickened and infiltrated. The 
 alveolar walls are very slightly infiltrated. They are filled with fluid and des- 
 quamated epithelial cfeUs and with dense plugs of fibrin which are in places or- 
 ganized. The organization does not extend to the bronchi. Certain areas show 
 the alveoli fiUed with leucocytes in a fibrin network, but these are only scattered 
 patches. Other areas are loaded with bacteria and are necrotic, the necrosis 
 involving the walls of the alveoli. Such bacteria are partly streptococci but 
 partly large Gram-positive spore-bearing baciUi. 
 
 Therefore the changes are probably in part due to postmortem decomposition. 
 Bacteriological cultures showed Gram-positive gas-producing bacilli in blood and 
 lungs. 
 
 Case 29. — C. B. D., age 20 yrs. Began Jan. 18 with nosebleed, cold in head, 
 and painful eyes, photophobia, fever, and chilliness. Entered hospital Jan. 23, 
 1918, with sore throat, reddened pharynx, no tonsillitis, a red crescentic papular 
 eruption over face and body. Coughing, with fine rales over the entire chest, per- 
 sisted. Rash lasted 5 or 6 days. Since onset patient has been hoarse and at pres- 
 ent (Feb. 4) cannot speak above a whisper. About Jan. 30 patient developed a 
 pain in both axillae with marked difficulty in breathing. Rales were heard over 
 both lungs. Inspiration lengthened and so labored as to bring in accessory 
 muscles. Friction rub in left axUla. The percussion note later became dull 
 or flat in the left axilla and back and the friction rub disappeared. Patient 
 growing more and more cyanotic, conscious, and very nervous. Needle inserted 
 at lower angle of left scapula but only blood obtained. Sputum abundant, greyish 
 white, tenacious. Patient died on Feb. 7, 9.50 p.m., 20 days after the onset of 
 measles. Cultures from sputum and material obtained from lung puncture 
 showed Streptococcus hcemolyticus . Blood culture taken Feb. 7 negative. Au- 
 topsy Feb. 8, 9 a.m. 
 
 Anatomical Diagnosis: Clinical history oj measles. Bilateral interstitial broncho- 
 pneumonia. Fibrinopurulent pleuritis {left). Early serofibrinous pericarditis. 
 
 Left pleural cavity. — Contains about 1,500 cc. of greenish brown turbid fluid. 
 The surfaces are covered with a fibrinous exudate, but as there are numerous ad- 
 hesions posteriorly most of the fluid is held in the anterior portion of the thorax. 
 Right pleural cavity. — There is no excess of fluid and the surfaces are smooth 
 anteriorly, but over the posterior part of the cavity and over the diaphragm the 
 lung is adherent by a thin hemorrhagic fibrinous exudate. Pericardial cavity. — 
 Contains about 40 cc. of slightly turbid fluid. The pericardial surfaces are slightly 
 injected and there are a few shreds of fibrin. Left lung. — The lung feels flabby 
 
58 PNEUMONIA IN ARMY CAMPS 
 
 and soft but contains some firmer nodules. The upper lobe is largely air-contain- 
 ing whUe the lower is heavy, dense, and collapsed. On section the upper lobe 
 shows very distinct interlobular septa, and in the upper posterior portion there 
 are a few small peribronchial consolidations surrounded by grey spongy tissue. 
 Several of these areas. are embedded in the deep red tissue of each lobule. In 
 the lower part of the lobe the consolidated portions are so numerous as to form 
 a confluent network. Each yellowish branching nodule is bordered with red and 
 these are separated by greyish tissue. In the lower lobe the mesial and posterior 
 parts are thickly studded with greyish yellow areas which in places grow large 
 and become confluent. In the outer or axiUary portion of the lobe these are 
 fewer and of smaller size. The septa are still conspicuous but the bronchi are 
 not. The lung is covered especially over the lower part with a thick fibrinous 
 exudate. Right lung. — The lung is voluminous and almost everywhere air- 
 containing. There is a thin fibrinous exudate over the lower lobe and lower 
 part of the upper. The bronchi are deeply reddened. The upper lobe is largely 
 air-containing. There are a few small branched peribronchial consolidations 
 and a large firm one 1 cm. in diameter. In the lower lobe there is no conspicuous 
 thickening of the bronchi, but in the lowermost part the bronchi are widened 
 and full of exudate and surrounded by feathery homogeneous, greyish red areas 
 of consolidation. From their homogeneous uniform appearance these seem to be 
 , areas in which the alveoli are filled with exudate. There are some large opaque 
 yellow patches and many confluent grey smooth areas. Larynx. — SKghtly red- 
 dened and covered with mucus. No ulceration visible. 
 
 Microscopic Examination. — The tissue of the left lung shows great thickening of 
 all the framework of the organ. The interlobular septa are wide, contain a good 
 deal of fibrin in the form of a network, but in most places this has disappeared 
 and the broad septum is made up of loose connective tissue with many fibroblasts. 
 The bronchi have lost their epithelium, contain leucocytes, desquamated epithe- 
 lium, and a few streptococci (Fig. 31). An effective stain reveals influenza bacilli 
 in great numbers in bronchi and alveoli. Elastic tissue stain shows readily the 
 original outlines, and it is clear that there is a thick layer densely infiltrated 
 with mononuclear cells which has formed just beneath the epithelium, lifting 
 it up. The remaining muscular and connective tissue portion of the wall is 
 densely infiltrated with mononuclear cells and some leucocytes and is much 
 thickened (Fig. 32). Viewed with a low power any one lobule appears denser 
 around the central bronchus and near the surrounding interlobular septa than in 
 the intervening zone. This is largely due to the fact that in the neighborhood 
 of the bronchus and at the periphery near the septum the alveolar walls are 
 greatly thickened. The epithelium is in general desquamated, but the underlying 
 structureless membrane which can be most distinctly seen is lifted away from the 
 capillaries which hold to the middle of the alveolar wall by a great mass of mono- 
 nuclear wandering cells and newly formed connective tissue. Thus in each al- 
 veolar wall the capillaries are covered on each side by a layer of these cells 
 
WILLIAM G. MacCALLTJM 59 
 
 bounded by the membrane of the wall. In the midzone of the lobule the alveolar 
 walls are thinner. All this infiltration and new connective tissue formation 
 forms another instance of the reason for speaking of this condition as interstitial 
 bronchopneumonia. 
 
 The alveoli contain many desquamated epithelial cells, rather dense fibrin, and 
 a few mononuclear wandering cells. There are few if any streptococci to be seen. 
 But in places there are small groups of alveoli densely filled with leucocytes 
 among which there are great numbers of streptococci. This coexistence of what 
 may be called lobular pneumonia with the interstitial bronchopneumonia is 
 noteworthy. The interlobular septa are composed of a network of fibroblasts 
 (Fig. 33). The lymphatics are wide and contain a mass of cells which are prac- 
 tically all mononuclear. Some are as large as alveolar epithelial cells. There is 
 often also a network of fibrin which is beginning to undergo organization. A few 
 streptococci are found there. 
 
 In other areas of the left lung and in the right lung the inflammatory process 
 beginning about the bronchi is associated with much edema and hemorrhage into 
 the alveoli. The left lung shows the most extreme interstitial changes yet seen. 
 There are quite large areas which are completely airless, the alveoli being filled 
 with fluid and desquamated cells and blood (Fig. 34), the alveolar walls, vessels 
 walls, and interlobular septa greatly widened by infiltration with mononuclear 
 cells. The lymphatics are filled with mononuclears and fibrin out to the pleural 
 exudate. The bronchi are enormously thickened and overvascularized. Usu- 
 ally the epithelium is lost and the thick wall densely infiltrated with mono- 
 nuclears. In some places the contents of the bronchi appear to be replaced by a 
 mass of newly formed vascular tissue. 
 
 The lobulated fat which hangs into the pleural cavity from the surface of the 
 pericardium is covered with exudate and most of the lobules are glued together. 
 Streptococci are abundant on the surface and extend into the ends of the open 
 crevices but are not found in the fibrin which closes the crevices or in the tissues. 
 
 Cultures from blood, pericardial fluid, pleural fluid, and left lung reveal Strep- 
 tococcus hcemolyticus. 
 
 Case 30.— F. E. H., age 23 yrs. Was in hospital for tonsillitis Dec. 24-29, 
 1917. No rash at this time. Since then has been having chills every night. On 
 Jan. 3 developed pain in the left side of the chest and entered the hospital, Jan. 
 6, 1918, with signs of dulness, tubular breathing, and crepitant rales over the 
 left lower chest. 1,000 cc. of turbid straw-colored fluid were aspirated on Jan. 
 21, and on Jan. 23 the left pleural cavity was drained by resection of the 7th 
 and 8th ribs. Leucocytes 35,000. Temperature 99-104° F., pulse 90-160, 
 respiration 20-40. Died Feb. 7, at 6 p.m. Autopsy Feb 8. 
 
 Anatomical Diagnosis: Interstitial bronchopneumonia and lobular pneumonia 
 with abscess formation and empyema {left side) . Lobular pneumonia {right lung) . 
 
 Left pleural cavity. — Obliterated by fresh adhesions in the anterior portion, but 
 posteriorly there is a cavity open to the air through an incision which interrupts 
 
60 PNEUMONIA IN ARMY CAMPS 
 
 the 7th and 8th ribs in the left anterior axillary line. This cavity contains about 
 400 cc. of an extremely foul greenish brown turbid fluid. The surfaces are covered 
 where they form the wall of the cavity with a thick greenish exudate. Right 
 pleural cavity. — Contains no excess of fluid and the surfaces are smooth and glisten- 
 ing. Left lung. — The lung is partly collapsed, its posterior part covered with 
 greenish exudate. The upper lobe contains a few small consolidated areas. The 
 lower lobe is closely studded with similar small consolidated patches which have 
 become liquefied centrally. The intervening lung substance is collapsed and ede- 
 matous. Right lung. — In general the lung is air-containing, but in the lower lobe 
 there are one or two firm nodules. One of these stands out above the surrounding 
 lung surface and the pleura over it is dull and covered with fibrinous exudate. 
 On section this patch is opaque and yellow, but it is still possible to discern in 
 it the bronchi filled with exudate. In other parts of the lung there are small 
 abscess-like foci surrounded by hemorrhage. 
 
 There are evident general signs of postmortem decomposition. The skin of 
 the abdomen is discolored and green and the gastric mucosa and retroperitoneal 
 tissues contain large gas blebs. 
 
 Microscopic Examination. — Sectiofis through the least affected part of the 
 left lung show the greatly thickened pleura which is replaced by a dense granu- 
 lation tissue. The bronchi are in places filled with an exudate of leucocytes and 
 mononuclears. The adjacent alveoli show slight infiltration of the walls; the 
 epithelial cells are desquamated and fill the lumen. Most striking is the pres- 
 ence of whole colonies of bacteria in the blood vessels and capillaries and some- 
 times in the alveoli and bronchi. Since these are present in enormous num- 
 bers in the capillaries of the liver, spleen, kidneys, and adrenals, with little or no 
 reaction about them, it seems probable that they have become so numerous 
 through postmortem growth. In other areas of the lung there are large patches 
 of necrosis in which all structure is lost and merged into a granular material 
 loaded with micrococci and masses of minute Gram-negative bacilli which may 
 be influenza bacilli. About these there is a dense pneumonic consolidation with 
 edema and hemorrhage in the distant margin. Many of the alveoli show a curious 
 columnar form of epithelium which makes them look like minute bronchioles. 
 
 No cultures were made. 
 
 Case 35. — C. E. P., age 26 yrs. Entered hospital Jan. 13, 1918, complaining 
 of pain in left chest, chiUs, and fever. No history of sore throat or rash. Does 
 not remember having had measles. Dulness with tubular breathing over the Igft 
 base at the back. Leucocytes 20,800. Temperature 101-105° F., pulse 120-160, 
 respiration 30-60. Jan. 26, evidences of fluid at the left base with new signs of 
 consolidation in upper left and lower right lobes. On Jan. 29 aspiration of the 
 right side gave 200 cc. of cloudy reddish brown fluid. Feb. 1, severe pain in 
 left chest. Feb. 5, rib resected on left side and drainage established after re- 
 peated aspirations during preceding 2 days. Feb. 9, patient complains of severe 
 pains in abdomen which is greatly distended, rigid, and very tender. No special 
 localization of tenderness. Died Feb. 10, 1918, at 10 p.m. Autopsy Feb. 11, 1918. 
 
WILLIAM G. MacCALLUM <51 
 
 Anatomical Diagnosis: Interstitial bronchopneumonia and lobular pneumonia with 
 empyema {left). Acute pericarditis {beginning). Acute generalized peritonitis. 
 Acute nephritis. 
 
 Upon opening the abdominal cavity there is an escape of turbid yellow fluid 
 with flakes of fibrin. The surfaces of the peritoneum are somewhat injected 
 on the left side but are everywhere smooth. No origin of this infection could 
 be found in the abdominal organs. Pericardium. — The pericardial sac contains 
 50 cc. of slightly turbid greenish yellow fluid. The vessels on the inner surface 
 of the parietal pericardium are slightly injected. Left pleural cavity. — There 
 is an incision in the anterior axillary line over the 7th rib and a portion of this 
 rib has been resected allowing fluid to escape through a rubber drainage tube. 
 Between the collapsed lower lobe of the lung and the parietal pleura there is 
 a cavity which contains about 400 cc. of a bloody purulent fluid. The upper 
 lobe is adherent over its whole surface excepting a small area posteriorly where 
 it forms part of the wall of the empyema cavity. The remaining pleural lining 
 where it forms the wall of this cavity is covered with a fibrinopurulent exudate. 
 Right pleural cavity. — Obliterated by very fresh light fibrous adhesions which 
 are easily broken through but which bind the lung to the costal pleura and 
 diaphragm. Left lung. — The pleura is much thickened and the lobes are bound 
 together by a fibrous layer 4 mm. in thickness. The lobes are heavy and air- 
 less except at the anterior margin of the upper lobe. On section the upper 
 lobe is dark red and rather edematous, but there are no areas of consolida- 
 tion. The lower lobe is also edematous on section and reddish grey in color. 
 The interlobular septa are prominent and in each lobule there are five or six 
 opaque yellow areas of consolidation many of which show a central cavity or 
 lumen. The bronchi in general are thick with reddened and edematous mucosa. 
 The surrounding tissue is dense and yellowish. The bronchial glands are en- 
 larged and soft. Right lung. — The surface is roughened and shows subpleural 
 hemorrhages and over the inferior border of the lower lobe a thick fibrinous exu- 
 date. All the lobes are readily insufflated, although the lower was collapsed 
 and heavy. In the upper and lower lobes and to a much less extent in the middle 
 there are found a few small greyish translucent areas which appear to be due to 
 thickening of the bronchioles. The bronchi are reddened. The lymph glands 
 at the hilum are swollen and soft. Kidneys. — Left kidney measures 12 by 5 by 4 
 cm. The capsule strips readily, leaving a smooth, pale greyish, opaque surface 
 upon which numerous small hemorrhages are to be seen. On section the cortex 
 measures 7 mm. in width. It appears swollen and opaque. The striations are 
 somewhat obscured by numerous small hemorrhages in the cortex. The glomeruli 
 are visible as small greyish dots. The pyramids are dark brownish red with very 
 distinct striations. Pelvis is normal. The right kidney is in all respects similar. 
 
 Cultures from the blood, pericardial fluid, pleural fluid, and left lung show 
 Streptococcus hamolyticus in pure culture. 
 
 Microscopic Examination. — The right lung in its lower lobe shows only rather 
 diffuse changes which consist in the filling up of the alveoli with fluid and blood. 
 
62 PNEUMONIA IN ARMY CAMPS 
 
 The walls are not especially altered, but in the capillaries there are surprising 
 numbers of megalocaryocytes. 
 
 Rather large bronchi shown in this section are loosely filled with leucocytes 
 and debris of epithelium. The bronchial wall is not markedly thickened, but it 
 is striking that in many places where the epithelium is desquamated there is a 
 distinct adherent layer of fibrin on the wall like a diphtheritic membrane. 
 
 The left lung, covered with a thick vascular layer of granulation tissue sur- 
 rounded by fibrin, is atelectatic, and the bronchi contain bacteria and pus. 
 There are no other remarkable alterations in this part of the lung. But in the 
 lower lobe the changes are advanced. The pleura is as just described. The 
 interlobular septa are wide and dense and contain lymphatics plugged with clots 
 made up of fibrin, leucocytes, and bacteria. The bronchi are dilated, the walls 
 greatly thickened by mononuclear infiltration, the epithelium is desquamated, and 
 the lumen fiUed with this and a mixture of fluid and leucocytes with bacteria. 
 Influenza bacilli are present in numbers among the streptococci. From the 
 region of the bronchi the alveolar walls are thickened by infiltration with 
 mononuclear cells and a great many leucocytes, but at a little distance this 
 thickening disappears. The whole tissue is compact and soKd because each 
 alveolus while partly collapsed contains desquamated epithelium, fluid, and 
 blood. There are not many mononuclear cells in the alveoli, but even in outlying 
 places they persist in the walls of the small blood vessels and adjacent alveoli. 
 
 There are many patches of lobular consolidation in which the alveoli are 
 tightly packed with leucocytes, which in places are entirely disintegrated and 
 appear as a dust of nuclear fragments. They are often surrounded by wide 
 zones of hemorrhage. These are areas of lobular pneumonia rich in bacteria, but 
 in contrast there are often found minute bronchioles which are filled with leuco- 
 cytes and whose walls are greatly widened by infiltration of mononuclears and 
 rendered so indefinite that their outlines cannot easily be recognized either 
 within or without. 
 
 The kidney shows very little change in the glomeruli. There "is occasionally 
 some coagulated fluid in the capsule. Epithelium of the tubules much degen- 
 erated and partly desquamated. The tubules are in places fiUed with blood and 
 leucocytes. There are a few leucocytes in the interstitial tissue. 
 
 Case 58. — M. F. M., age 25 yrs. History negative. Present illness began on 
 Jan. 10, 1918, with a severe cold accompanied by sore throat, headache, and 
 fever. Began to have pain in his left side on the day of admission to the hos- 
 pital, Jan. 13. Dulness was found over both lower lobes but there were no 
 rales and brea,th sounds were faint. Temperature ranged from 101-104.8° F., 
 pulse 120-130, and respiration 28-48 until Jan. 28, when temperature fell to 
 normal. There was marked delirium on Jan. 18. Pus was aspirated from the 
 right chest on Jan. 27, and the next day the 7th rib was resected and the right 
 pleura drained. The temperature remained rather high, 100-102°, and the pa- 
 tient was occasionally delirious until his death on Mar. 8, 1918. Autopsy Mar. 
 8, 1918. 
 
WILLIAM G. MacCALLUM 63 
 
 Anatomical Diagnosis: Old interstitial bronchopneumonia with empyema {right). 
 Abscess of lung- Acute perilotiitis . 
 
 Left pleural cavity. — Contains no fluid but there are light fibrinous adhesions 
 on the back of each lobe. The lower lobe is adherent to the diaphragm and 
 there are slight fibrinous adhesions on the anterior margin of both lobes. Right 
 pleural cavity. — In the right anterior axillary line there is a large operative 
 wound over the 6th rib. The margins are covered with granulation tissue and 
 a large piece of the underlying rib has been resected. The lung can be seen 
 to be collapsed. The pleural surfaces are thickened and reddened and covered 
 with a soft fibrinopurulent exudate which overlies a layer of granulation tissue. 
 The cavity contains about 300 cc. of very foul pus. Left lung. — The whole lung 
 can be inflated artificially and on section is found to be air-containing every- 
 where with the exception of a few areas in the lower posterior portion of 
 the upper lobe and a few in the lower lobe. These are grouped together, 
 two and three being found in each lobule. They have a central lumen which 
 is fiUed with a yellow purulent fluid, and are surrounded by a hemorrhagic 
 zone. The bronchi contain a sticky mucoid material, and the mucosa is hem- 
 orrhagic. The interlobular septa are not thickened. Bronchial glands only 
 slightly enlarged. Right lung. — Completely collapsed and pressed against the 
 vertebral column. It is densely adherent to the diaphragm by fibrous ad- 
 hesions. Over the anterior surface of the upper lobe is a large necrotic area, 
 irregular in form and measuring 8 by 6 cm. which is covered by dirty, foul 
 smelHng, greenish yellow exudate. On section this mass replaces about half 
 the upper lobe. Its central part is softened, very foul, and yellowish green in 
 color, and this condition radiates out into the surrounding lung substance. The 
 rest of the upper lobe is airless, dark grey, and rather granular in appearance. 
 There are numerous thickened edematous interlobular septa, and in the lobules 
 so outlined the branches of the small bronchi filled with yellow exudate are promi- 
 nent. One such group in the posterior part of the lobe is surrounded by a hemor- 
 rhagic zone. The lower lobe is also heavy, airless, and flabby. In the posterior 
 part there are several lobules which are pale grey and quite airless, in which there 
 are peribronchial nodules. These lobules are sharply outlined by the inter- 
 lobular septa. Pericardium. — Contains 30 cc. of turbid fluid with floating 
 shreds of fibrin. The pericardial surfaces are, however, still glossy. Heart is 
 normal. 
 
 Culture from the blood gave a Gram-positive streptococcus, but this was 
 overgrown by putrefactive bacilli. 
 
 Microscopic Examination. — The pleura over the right lung is extremely thick 
 and dense with radially placed blood vessels and an overlying layer of fibrin 
 on the surface of which are great quantities of bacteria. 
 
 Most of the sections show wide and rather dense interlobular septa running 
 into the lung substance. Most of the fibrin and fluid in these are absorbed 
 and only remnants of dense red-staining fibrin remain. The lymphatics are 
 
64 PNEUMONIA IN ARMY CAMPS 
 
 hard to find, but where they can be outlined they are distended with a mass of 
 new connective tissue infiltrated with cells. Evidently the thrombi with abun- 
 dant leucocytes and bacteria have in this case been organized in the same way 
 as the contents of the alveoli and replaced by connective tissue. The septa 
 themselves are composed of rather dense fibrous tissue with many wandering 
 cells. 
 
 The bronchi retain their epithelium and are filled with leucocytes in most 
 cases, but their walls are greatly thickened and have the appearance of a layer of 
 granulation tissue with abundant wide blood vessels running radially. They are 
 densely infiltrated with wandering mononuclear cells. The alveolar walls are 
 similarly thickened. Over large areas they are quite collapsed. In others they 
 contain dense fibrin which is often in an advanced stage of organization. Most 
 of them contain fluid and abundant desquamated epithelial cells. There are 
 areas too in which these changes are not developed but in which the bronchi and 
 alveolar walls remain thin and the alveoli are filled with fluid and with poly- 
 morphonuclear leucocytes. 
 
 In the districts in which the alveoli and bronchi are most thickened there 
 are large irregular abscesses which send off long prolongations and are marked 
 out by a dense wall of fibrin with fragmented nuclei. Within these walls the 
 whole substance of the lung has been broken down, shreds of elastic tissue remain, 
 but the rest is seen in the form of a necrotic debris with great numbers of bac- 
 teria. It is not possible to maintain in this case that the formation of such an 
 abscess occurs only in an area of lobular pneumonia; on the other hand the 
 areas of leucocytic exudate show none of the abscesses. 
 
 One receives the impression that this is a protracted case of interstitial bron- 
 chopneumonia lengthened in its course by the persistence of the empyema and 
 that in some senses an advance toward healing has occurred, especially in the 
 organization of the exudate in alveoli and lymphatics. But the occurrence of 
 large abscesses has interfered with the completion of this process. The whole 
 arrangement of the lymphatics must be greatly altered by such a process, and if 
 recovery had occurred new lymphatics must have been required. 
 
 Case 176. — A. G., age 24 yrs. Began on Mar. 25, 1918, with measles. On 
 Apr. 6 complained of pain in the right side, and physical examination on 
 Apr. 10 resulted in the diagnosis of lobar pneumonia involving the right lower 
 and middle lobes. On Apr. 1 1 empyema was recognized on the right side and an 
 operation was performed with resection of the 9th rib and drainage of the pleural 
 cavity. Died May 9, 1918, at 6 a.m. The chnical diagnosis at the time of 
 death was lobar pneumonia, the right lower lobe resolving. Bronchopneumonia 
 (left); bilateral empyema. Acute pericarditis and myocarditis. Culture from 
 the blood on Apr. 28 was sterile. On Apr. 11 culture from the pleural exudate 
 gave Streptococcus hamolyticus . Autopsy May 9, 1918, at 11 a.m. 
 
WILLIAM G. MacCALLUM 65 
 
 Anatomical Diagnosis: Clinical history of measles. Lobular pneumonia (right) 
 with old empyema. Fresh fibrinopurulent pleuritis (left) . Subacute purulent peri- 
 carditis with adhesions. Acute serofibrinous peritonitis. Phlegmonous infiltration 
 of neck. 
 
 Left pleural cavity. — Contains 500 cc. of thick turbid, slightly blood-stained 
 brownish fluid. The costal pleura is covered with yellow fibrin which over- 
 lies a velvety red pleural membrane. The lung is plastered against the peri- 
 cardium and is adherent along the vertebral column to its apex. Otherwise 
 it is everywhere free, but the fibrin is especially thick between the lung and dia- 
 phragm. Right pleural cavity. — In the right back 3 cm. below the angle of the 
 scapula there is a wound about 7 cm. long rising in an oblique direction along 
 the line of the 9th rib. The ends of the rib project through the granulating 
 wound. The pleural cavity is free from adhesions anteriorly from apex to 
 diaphragm, back to the midaxillary line where it is obhterated above the 6th 
 rib by adhesions, and below that level opens out into a large cavity which extends 
 back to the vertebral column. This space is lined with granulation tissue and 
 fibrin and into it the wound in the back opens. Pericardial sac. — Greatly thickened. 
 The anterior wall is fully 6 mm. in thickness and is lined with a layer of trans- 
 lucent tissue about 4 mm. thick which contains opacities. The cavity is partially 
 obhterated, but the remaining space contains about 40 cc. of thick creamy pus 
 which is pale greenish yellow in color and contains thick clumps of yellow fibrinous 
 material. Peritoneal surfaces. — Have lost their gloss to some extent and there is 
 some turbid fluid with flakes of fibrin in various dependent parts. Left lung. — 
 Almost entirely collapsed and blue and flabby. The whole lung can be inflated 
 and on section presents a normal texture without consohdation and with prac- 
 tically normal bronchi. There is a small part of the lower lobe posteriorly which 
 fails to become inflated. Right lung. — The surface is changed in appearance by 
 the alterations of the pleura already described. The bronchial glands are en- 
 larged and opaque grey in color. The upper lobe contains air throughout; 
 it is normal in texture and there are no areas of consolidation. The middle lobe 
 is partly atelectatic but nowhere consolidated. The lower lobe contains air in 
 its upper part, but the lower part is collapsed. In this collapsed part there is a 
 group of small areas of consohdation which are grey on a greyish red background, 
 more or less confluent and irregular in outline. They seem not distinctly peri- 
 bronchial, but to consist of alveoli filled with exudate. In the more posterior 
 part of the lobe there are even more distinct grey areas of consolidation in which 
 plugs of exudate can be seen in each alveolus. The bronchi and blood vessels 
 are not thickened, but the interlobular septa are rather prominent. Tonsils, 
 larynx, and pharynx. — Fairly normal. There is a multilocular abscess in the 
 intermuscular spaces of the left side of the neck extending up as far as the mas^ 
 toid with which it has no apparent connection and down behind the clavicle to 
 the pleura with which it does not communicate. The right shoulder joint is in- 
 
66 PNEUMONIA IN ARMY CAMPS 
 
 tact, but the abscess extends between the scapula and the vertebral ends of the 
 upper ribs for a long distance. 
 
 Cultures from both lungs, left pleura, pericardium, and from the abscess in 
 the neck gave Streptococcus hcemolyticus. Culture from the heart's blood was 
 sterUe. 
 
 Microscopic Examination. — The substance of the lower lobe of the right lung 
 presents the only remarkable change. The pleura is greatly thickened and con- 
 verted into a rather dense granulation tissue with overlying fibrin. The in- 
 terlobular septa are extraordinarily wide and rather dense. They appear to 
 represent old changes. The lymphatics which run in these are distended with 
 cells which are partly leucocytes, partly mononuclear cells, and this material is 
 loaded with Gram-positive cocci which are far more numerous here than else- 
 where. They a,re usually in pairs and only rarely in longer chains. The bronchi 
 are slightly thickened and their walls moderately infiltrated with cells which are 
 in part polymorphonuclear leucocytes. They contain a purulent exudate which 
 is full of streptococci. No influenza bacilli are foimd. The alveolar walls are 
 slightly thickened, in many places not at all. They are infiltrated in places with 
 leucocytes, but near the blood vessels they may be filled with mononuclear cells. 
 On the basis of this rather slight interstitial change there is a distinct intra- 
 alveolar exudate of red corpuscles, leucocytes in great numbers, and fibrin. It 
 constitutes a definite lobular pneumonia. The bacteria are present among the 
 polymorphonuclear leucocytes, but not in great numbers and not more distinctly 
 in chains than elsewhere. In the margin or tip of the lower lobe there is a 
 peculiar change. The interstitial tissue is greatly increased and infiltrated with 
 leucocytes and fibrin. The alveoli appear as rather widely separated spaces in 
 this tissue and either have no lining or are lined with thin scale-hke epithelium. 
 The bronchioles with their columnar epithelium similarly appear isolated in the 
 dense tissue. 
 
 Sections of the connective tissue and muscle about the abscess of the neck 
 show great numbers of streptococci in necrotic tissue and in the crevices of a 
 difliuse granulation tissue. 
 
 Case 181.— E. J., age 26 yrs. Began Mar. 24, 1918, with bronchitis. Onset 
 rather sudden with chills, fever, headache, weakness, and general malaise. 
 Scattered rales heard over lungs. On Mar. 31 subcrepitant rales and bronchial 
 breathing over the left lower lobe posteriorly. On Apr. 1 a small area of con- 
 solidation in the right lower lobe in the axillary line. On Apr. 16 no definite 
 signs over the lungs. Aspiration of right axilla negative. Apr. 19, suppurative 
 otitis. Crepitant rales and slightly diminished resonance over whole right side 
 anteriorly. Apr. 21, impaired breathing over right lower lobe. Apr. 26, 200 cc. 
 of limpid greenish yellow fluid aspirated from right upper chest. This fluid 
 contained Streptococcus hcemolyticus as shown by culture. Flatness over this 
 region next day. May 5, aspirated 300 cc. from right chest. Culture from 
 pleural fluid on May 10 gave Streptococcus hcemolyticus. Died May 10, 1918, at 
 2.15 p.m. Autopsy May 11, 1918, at 10 a.m. 
 
WILLIAM G. MacCALLUM 67 
 
 Anatomical Diagnosis: Interstitial bronchopneumonia (bilateral) with abscess for- 
 mation and empyema {right) . Lobular pneumonia {left) . 
 
 Left pleural cavity. — Contains no fluid. Surfaces smooth. Right pleural cavity. 
 — Contains 400 cc. of thick greenish mixture of fibrin and pus which will hardly 
 pour. The right lung is plastered against the pericardial sac. The apical part of 
 the lung is adherent along the 3rd rib laterally, but otherwise the pleural surfaces 
 are held apart. They are covered with a thick yellowish shaggy layer of fibrin. 
 Left lung. — The lung is voluminous with smooth, glistening surfaces, but some 
 small nodules can be felt in its substance. The upper lobe is easily inflated and on 
 section is normal in texture. The lower lobe is also easily distended, but poste- 
 riorly and below there are some small greyish yellow nodular consolidations. 
 Right lung. — The organ is collapsed, pasty, and heavy, and one may palpate 
 nodular consoUdations in its substance. On section there is found a cavity 
 about 3 cm. in diameter in the substance of the upper lobe (Fig. 35). This ex- 
 cavation is fuU of purulent material and is in open communication with a large 
 bronchus whose walls it has abruptly interrupted. There is no communication 
 with the pleural space. The lung tissue surrounding this cavity is irregularly 
 consolidated. The interlobular septa are conspicuous. The lower lobe shows the 
 bronchi widely dilated to the periphery and fiUed with purulent material. About 
 these there are areas of consohdation which become confluent so that practically 
 the whole posterior part of the lower lobe is airless, the smooth firm areas being 
 separated in places by only a narrow line of air-containing tissue. Pharynx and 
 larynx. — The pharynx is not especially reddened. The larynx including epi- 
 glottis and vocal cords is pale, smooth, and normal throughout. The mucosa of 
 the trachea is pale. 
 
 Cultures made at autopsy show Streptococcus hcemolyticus in the heart's blood, 
 both lungs, and right pleura. 
 
 Microscopic Examination. — The left lung shows a thin smooth pleura. The 
 interlobular septa are not thickened and the lymphatics are inconspicuous. 
 There is a widespread filling of the bronchioles with purulent exudate. The 
 walls are moderately thickened and hyperemic and infiltrated with mononuclear 
 cells. This alteration is relatively shght, however, and the corresponding changes 
 in the adjacent alveolar walls are also very slight. StUl there are areas about 
 many of these bronchi in which the alveoli are filled with thick fiuid, with blood, 
 and desquamated epithelial cells. Most of the bronchi are surrounded, however, 
 by small groups of alveoli which contain a dense exudate of leucocytes with deli- 
 cate network of fibrin and very httle blood. There are many streptococci among 
 these leucocytes, and numerous influenza bacilli. 
 
 The right lung shows a thick pleura covered with granulation tissue and 
 fibrin. The interlobular septa and indeed all the connective tissue structures 
 throughout the lung are enormously thickened and rendered dense by a new 
 growth of tissue. 
 
 The bronchi are greatly distended and filled with a solid mass of leucocytes. 
 Their walls still show in most places the layer of epithelium, but some of them 
 
68 PNEUMONIA IN ARMY CAMPS 
 
 are completely denuded. In general the bronchial walls are greatly thickened 
 and converted into a vascular granulation tissue which is densely infiltrated with 
 mononuclear cells. The alveoli are practically all collapsed, their walls greatly 
 thickened and infiltrated, but there is not much beyond a few alveolar epithelial 
 cells in their cavities. The lymphatics are. nowhere conspicuous, and many of 
 them have probably been obliterated. 
 
 This case exhibits, therefore, an old interstitial bronchopneumonia with great 
 dilatation of the bronchi and induration of the framework of the lung, with 
 empyema causing a collapse, and necrosis and cavity formation in the upper lobe. 
 All this affects the right lung while the left lung is studded with patches of 
 lobular pneumonia in a tissue in which there are traces of the interstitial process. 
 
 Case 194. — J. J., age 25 yrs. Negro. Had measles on May 3, 1918. On ad- 
 mission, May 9, riles at both bases. Lobar pneumonia of right lower lobe recog- 
 nized May 10, 1918. May 13, dulness of right lower lobe with riles; hoarseness. 
 On May 16 fluid was suspected in the right chest and peritonitis was also diag- 
 nosed. Right lower lobe very duU; breath sounds distant. Sputum on May 
 13 was yellow, mucopurulent, and contained Gram-positive cocci which proved 
 to be Staphylococcus aureus and Streptococcus hcemolyticus. Influenza baciUi 
 were also there. Died May 16, 1918, at 1 p.m. Autopsy May 16, 1918, 2 
 hours after death. 
 
 Anatomical Diagnosis: Early interstitial bronchopneumonia {left), with lobular 
 pneumonia. Empyema with collapse of lung {right) . Acute fibrinopurulent peri- 
 tonitis. Acute splenic tumor with hemorrhagic infarctions. Ulcerative laryngitis. 
 
 Peritoneum. — Contains a yellow fluid with flakes of fibrin which is plastered 
 on the abdominal organs. The pelvis contains a purulent fluid. Left pleural 
 cavity. — Contains no excess of fluid, but the surfaces are roughened by a fresh 
 fibrinous exudate. Right pleural cavity. — This side contains a great deal (2.5 
 liters) of turbid fluid much of which is imprisoned in a space between the lung, 
 diaphragm, and pericardial sac. The fluid is brownish and turbid with a thick 
 sediment. Left lung. — The lung is voluminous (Fig. 36). The surfaces are 
 smooth except at the posterior part of the lower lobe where the pleura is deep 
 purphsh and covers an area which is firm and nodular. The upper lobe is air- 
 containing throughout and normal in texture. The bronchi are not altered. 
 The lower lobe is thickly studded with small greyish nodules which correspond 
 with the terminations of the bronchi and are surrounded by bright red hemor- 
 rhagic areas. In the lower posterior part of the lobe there are confluent hemor- 
 rhages within which there are several dry, opaque, dull red patches which stand 
 up a little above the surface. The bronchi are widened a little and contain a 
 bloody, frothy, grey exudate. Their walls are deeply congested. The bronchial 
 glands are greatly enlarged, edematous, and grey. Right lung. — The right lung 
 is collapsed into a wrinkled soft mass. The lobes are somewhat adherent, and 
 on pulling them apart small cavities in the fibrin, containing green pus, are torn 
 open. The lung can be artificially inflated and then on section the whole lung 
 
WILLIAM G. MacCALLUM 69 
 
 is found to be air-containing. The cut surface is smooth and satiny. The 
 bronchi are reddened and contain only frothy fluid. The bronchial glands are 
 large. Pharynx and larynx. — Tonsils not enlarged. Epiglottis is pale. The 
 vocal cords are distinctly ulcerated along their edges, but the rest of the larynx 
 seems normal. Spleen. — Enlarged, measuring 16.5 by 12.5 by 5 cm. It is 
 irregular in consistency and on section there are dark red, dry looking areas 
 which are firmer than the rest and extend deep into the spleen. It is impossible' 
 to make out any plugs in the vessels; in fact liquid blood can be squeezed from 
 the vessels in the centers of these areas. The Malpighian bodies are pretty well 
 seen throughout the cut surface. 
 
 Cultures made at autopsy showed Streptococcus hamolyticus in the heart's 
 blood, right and left lung, right pleura, and peritoneum. The streptococci were 
 mixed with many other organisms in the smear from the ulcer of the vocal cord. 
 The right lung gave also Staphylococcus aureus. 
 
 Microscopic Examination. — The diaphragm shows an exudate of fibrin and 
 leucocytes on both sides. That on the pleural surface is dense and compact 
 while that on the peritoneal side is very loose. The absorbent lymphatics in 
 the peritoneal surface are packed with leucocytes and such dense thrombi can 
 be tracked into the larger lymphatics which extend to the pleural surface. It 
 seems probable that the infection is transmitted from pleura to peritoneum by 
 way of the lymphatics against the ordinary course of their stream which be- 
 comes possible when they are thus obstructed by a thrombus in which the bac- 
 teria are growing. It is analogous to the condition in the lung which leads to 
 empyema. 
 
 In the left lung most of the tissue is properly air-containing, but there are 
 scattered bronchi which contain purulent or bloody exudate whose waUs are 
 thickened and infiltrated. They are surrounded by a group of alveoli whose 
 walls are similarly infiltrated, while their cavities are filled with leucocytes or 
 desquamated epithelial cells. They together with the adjacent alveoli contain a 
 great quantity of blood. Some of these patches are overwhelmingly filled with 
 blood so that it is difficult to see anything else, while others have the alveoli 
 filled entirely with polymorphonuclear leucocytes. The latter places are loaded 
 with streptococci which are much more numerous there than in the more intensely 
 hemorrhagic patches. There are also some rather large Gram-positive baciUi 
 in the affected parts of the tissue and these are found in numbers in the hemor- 
 rhagic areas. The dull red dry patch in the lower part of the lobe is found on 
 section to be in large part necrotic. The nuclei of the alveolar walls no longer 
 stain, but the walls are yet traceable through the solid mass of blood. The cap- 
 illaries can be seen to be much distended. The bronchi are widened and thick- 
 ened by infiltration and contain streptococci, although there are not many 
 organisms in the hemorrhagic tissue. The blood vessels contain dense clots, but 
 they have not definitely the architecture of thrombi. All the alveoli in this 
 neighborhood contain some leucocytes, but there are regions in which their cavi- 
 ties are closely packed with leucocytes among which streptococci are found. 
 
70 PNEUMONIA IN ARMY CAMPS 
 
 The right lung shows practically no alteration of the tissue. The bronchi are 
 thin walled and not infiltrated. The pleura is, however, thickened by the for- 
 mation of a granulation tissue and the section shows one of the interlobar en- 
 capsulated pockets which is lined with a thickened pleura and fibrin in the same 
 way. The immediately adjacent tissue is stUl collapsed and perhaps somewhat 
 indurated. - 
 
 Case 205.— R. W., age 29 yrs. Negro. Began on May 4, 1918, with measles. 
 Later was transferred to pneumonia ward with signs of bronchopneumonia in- 
 volving both lungs on May 7, 1918. Sputum contained Streptococcus hcsmolyticus 
 and influenza bacillus. Blood culture on May 8 was sterile. On May IS otitis 
 media developed in both ears and the patient became very deaf. Died May 20, 
 1918, at S.50 p.m. Autopsy May 21, 1918. 
 
 Anatomical Diagnosis: Interstitial bronchopneumonia and lobular pneumonia 
 {bilateral) . Empyema {right) . Bilateral symmetrical rupture of rectus abdominis. 
 Suppurative otitis media {bilateral) . 
 
 On incision through the anterior abdominal wall a cavity is found in the rectus 
 abdominis at the junction of the lower and middle third of the muscle. This is 
 due to a rupture of the muscle which leaves a space 4 cm. in diameter filled with a 
 bloody fluid. There is a similar hemorrhagic cavity in the opposite muscle at 
 exactly the same level (Fig. 37). On section the ends of the muscle are deeply in- 
 filtrated with blood and are dark red and opaque. The lower fragment is distinctly 
 yellow. The hemorrhages bulge into the peritoneal cavity and fluctuate, but there 
 is no excess of fluid in that cavity nor any hemorrhage, and the peritoneal surface 
 of the bulging masses is smooth. Left pleural cavity. — Contains no excess of fluid. 
 The surfaces are smooth. Right pleural cavity. — The cavity contains 400 cc. of 
 turbid brownish fluid in which float flakes of fibrin. The surface of the lung is 
 gelatinous and covered thickly with slimy patches of fibrin. There are a few small 
 hemorrhages. Left lung. — The lung is voluminous and appears to contain some 
 air everywhere. It is readily inflated artificially. On section the upper lobe is 
 found to contain numerous small nodular areas of grey consolidation not especially 
 surrounded by hemorrhage but apparently surrounding the terminal parts of the 
 bronchi. They measure 2 to 6 mm. in diam^er and become more numerous in the 
 posterior part of the lobe. They are nowhere confluent. In the lower lobe the 
 same condition exists and the nodules are extremely numerous in the posterior 
 part of the lobe (Fig. 38). Right lung. — The lung is heavy and pasty and dark 
 reddish purple in color. The bronchial glands at the hilum are very much en- 
 larged. The pleural surface is roughened by fibrin. The anterior portions of the 
 upper and middle lobes are air- containing. The posterior portions and the 
 lower lobe are collapsed. On section the whole lung is thickly studded with 
 grey peribronchial nodules becoming more abundant in the posterior parts. 
 The interlobular septa are prominent, marking out the lobules, and each lobule 
 contains several nodules. There is in the lower lobe a large wedge-shaped 
 area running back to the posterior border in which the nodules are not 
 
WILLIAM G. MacCALLXJM 71 
 
 surrounded by air-containing tissue but are broad and confluent forming a 
 greyish red area in which more opaque yellow patches are visible (Fig. 39). The 
 bronchi are dilated and their mucosa is reddened. Pharynx and larynx. — The 
 posterior nares and pharynx are reddened. The tonsils are normal. The vocal 
 cords are rather deeply ulcerated throughout most of their length. The mucosa 
 of the trachea is reddened. Middle ear. — On exposing the cavities both middle 
 ears are found to be fiUed with pus. 
 
 Cultures at autopsy showed Streptococcus hcemolyticus in the heart's blood, 
 both lungs, and right pleura, also in the right middle ear, but the bloody fluid 
 from the ruptured rectus abdominis gave no growth. 
 
 Microscopic Examination. — The conditions found throughout the two lungs 
 are about the same. 
 
 The pleura is thick on the right side and covered with rather homogeneous 
 fibrin. The interlobular septa are as a rule not very conspicuous, but some of 
 them contain large lymphatics distended with a mass of leucocytes which are 
 usually almost necrotic and disintegrated into a poorly staining debris. 
 
 The bronchi are fiUed with a similar mass of granular and fragmented leuco- 
 cytes containing streptococci and influenza bacilli. The walls are greatly 
 thickened, hyperemic, and densely infiltrated with mononuclear cells. In most 
 places the epithelium has been destroyed and a necrotic layer forms the lining. 
 The surrounding tissue is edematous, but the nearby alveoli are filled with 
 desquamated epithelial cells, mononuclear wandering cells, blood, and leucocytes. 
 In places the leucocytes predominate and produce patches of what would be 
 recognized as a lobular exudative pneumonia. Here, too, the leucocytes are 
 much disintegrated. But in most places this exudative type is not found and 
 the lesion is essentially that so often described as interstitial bronchopneumonia. 
 The thickening of the alveolar walls is relatively slight, but the lining epithelium 
 tends to be cubical and is evidently in proliferation. 
 
 The rectus abdominis muscle shows a mass of blood clot in contact with the 
 ruptured end where necrotic hyaline muscle tissue alone is found. AU through 
 the muscle, however, in diminishing degree as one passes away from the point of 
 the rupture there are extreme alterations which consist in the conversion of the 
 muscle fibers into hyaline material. This looks like an old process. Each 
 clump is surrounded by a mass of nuclei which are probably sarcolemma nuclei 
 which have been concentrated. In places these look like wandering cells, but 
 they are fairly well limited to the surrounding sheath of each hyaline clump. 
 A separate and more detailed study of these muscular changes must be made. 
 
 This group of cases is not sharply distinguished from the preced- 
 ing, since many of those showed a few foci of lobular pneumonia, but 
 it is separated because it is desired to show that this combination is 
 possible in an advanced degree. It may possibly represent a stage in 
 the whole process at which the lung which is the seat of a lesion in the 
 
72 • PNEUMONIA IN ARMY CAMPS 
 
 production of which the tissues have evinced a marked power of re- 
 sistance finally fails so that the organisms invade more readily. But 
 not much stress can be laid upon this suggestion since these lesions 
 seem to develop side by side in some cases of brief duration. 
 
 Dr. Allen Krause has suggested that in a person already tubercu- 
 lous the sudden appearance of a tuberculous pneumonia is probably 
 due to hypersensitization of the individual by the old tuberculosis, 
 so that the introduction of bacteria into a fresh bronchus results in 
 pneumonic infiltration in a way that could not happen in a normal 
 non-sensitized person. It seems possible that this suggestion might 
 be transferred to the case of this combined form of streptococcal 
 pneumonia. We have observed the anatomical difference between 
 the lesions and especially the type of distribution of bacteria in the 
 two forms and have found that in a lung in which in general the 
 streptococci are limited to bronchi and lymphatics there suddenly 
 appear patches in which the alveoli are filled with bacteria and with 
 leucocytes which tend to act toward them as phagocytes. We have 
 spoken of this as a final failure of resistance — ^possibly the failure of 
 resistance has through the action of the poison of the original 
 infection become an actual welcome to the invaders. 
 
 In Cases 181, 205, and 29 there were influenza bacilli in the bron- 
 chial exudate. These must be looked upon as possible participants 
 in the production of the interstitial changes. Indeed, except for the 
 occurrence of advanced lesions of this type in cases in which the 
 streptococcus is present alone (Nos. 34, 41, 178, and 184), it would 
 be difficult to insist that the influenza bacillus is not regularly the 
 cause of the interstitial changes. 
 
 In its gross appearance such a lung resembles closely those just 
 described. Nevertheless one may recognize here and there on the 
 cut surface irregularly outHned areas which are solid, dull and 
 opaque, and rather dry looking, grey or greyish red, and generally 
 accompanied by a wide zone of hemorrhage. Such areas can be 
 seen in the lungs of Cases 194, 184, 178, and others. 
 
 On microscopic examination these prove to be areas in which the 
 interstitial changes described before which lead to the thickening of 
 the alveolar walls are absent. Thickened bronchi and widened inter- 
 lobular septa may pass nearby, but in these areas the alveoli are thin 
 
WILLIAM G. MacCALLUM 73 
 
 walled and widely distended or packed with an exudate which is 
 composed chiefly of polymorphonuclear leucocytes in a delicate net- 
 work of fibrin. Blood corpuscles are present in small numbers and 
 in far greater numbers in the adjoining or marginal alveoli. The 
 most interesting feature is found in the distribution of the strepto- 
 cocci which are present in great numbers all through the exudate, 
 usually in pairs or short chains or even singly. They lie ever3nvhere 
 among the leucocytes, often within some of the cells which have 
 acted as phagocytes, but usually free. It is noteworthy that in most 
 of these cases the leucocytes forming the exudate in the alveoli show 
 signs of disintegration. In places their nuclei stain indefinitely or 
 are fragmented and the outlines of the cells have become extremely 
 indistinct. In some cases, as in No. 194, there are areas of necrosis 
 involving the alveolar walls and surrounded by hemorrhage. 
 
 Other areas of lobular consohdation containing the streptococci 
 in numbers are surrounded by zones of edema in which the alveoli 
 contain only fluid in which float a few chains of streptococci. 
 
 These cases show also pecuHarly well the lesions of the interstitial 
 bronchopneumonia, sometimes very fresh as in Cases 178 and 184, 
 sometimes old as in Cases 29, 58, and 181. In the last of these, No. 
 181, there is extensive bronchiectasis in the lower lobe and a cavity 
 in communication with a bronchus in the upper lobe of one lung, 
 while the opposite lung is studded with foci of lobular pneumonia 
 together with the fresher stages of the interstitial change in the 
 bronchi. 
 
 Such lobular lesions appear, however, in their most destructive 
 form in the third group of cases in which they are not combined with 
 the interstitial changes. 
 
 3. Lobular Pneumonia. 
 
 Case 20.— J. C, age 22 yrs. Entered hospital Jan. 28, 1918, complaining of 
 headache, rash, and pain in the eyes. Symptoms of 8 hours duration. Very 
 faint papular rash on chest, arms, and face. Conjunctivae injected, pharynx 
 red, Kophk's spots present. No dulness, but fine moist rales throughout both 
 lungs. Temperature 101-106° F., pulse 100-140, respiration 20-50. Died Feb. 
 4. Autopsy 2 hours later. 
 
74 PNEUMONIA IN ARMY CAMPS 
 
 Anatomical Diagnosis: Confluent lobular pneumonia with abscess formation. 
 Hemorrhagic serofibrinous pleuritis. Hemorrhagic lobular pneumonia {left lung). 
 Left pleural cavity. — Contains no excess of fluid and the surfaces are smooth 
 and glistening. Right pleural cavity. — Contains about 1,500 cc. of turbid greenish 
 fluid with some floating fibrin. The surface of the right lung is red and dull 
 looking, and this appearance seen also on the parietal pleura is due to intense 
 injection of the blood vessels and minute hemorrhages. There is very little de- 
 posit of fibrin. The lung is much collapsed but floats upon the surface of the 
 fluid. Left lung. — Very voluminous with smooth surface but mottled posteriorly 
 with dark red platelets. It is somewhat collapsed. The anterior portion is 
 air-containing, the posterior portion thickly studded with slightly elevated dry 
 hemorrhagic patches from 2 to 5 mm. in diameter. In these areas there is no 
 very definite consolidation, there is no yeUow opacity nor any solid nodule, nor 
 can distinct alveolar plugs of exudate be seen. Bronchi are not definitely seen 
 in the centers. Right lung (Fig. 40). — Adherent to a slight degree. It is al- 
 most entirely collapsed. In the posterior part of the lower lobe there is a large 
 solid mass about 8 cm. in diameter, which is seen through the pleura to be purplish 
 black in color. There are a few small rounded or branched opaque yellow areas 
 which shine through. On section the lung is very deep red throughout, but the 
 firm area in the lower lobe is almost black and a quantity of turbid bloody fluid 
 exudes from it. In the upper lobe which is fairly easily insufflated there are 
 many small irregular patches of grey consolidation in which each alveolus con- 
 tains a plug of exudate. These are duU brownish grey, dry, and hemorrhagic. 
 In the lower lobe there are many confluent areas of this sort often showing cen- 
 tral bronchioles. They are greyish red and the intervening lung is hemorrhagic 
 and solid. Each blood vessel is sheathed in a great wide mantle of yellowish 
 white suggesting distension of the adventitial lymphatics with purulent exudate. 
 Toward the lower margin such beaded yellow strands run out in the interlobular 
 septa to the pleura where they spread out as yeUow networks immediately under 
 the surface. Some are quite large and in the depth of the lung show softened 
 centers like abscesses. There is no fibrinous exudate on the surface. Bronchial 
 glands slightly enlarged with some pigmentation. 
 
 Microscopic Examination. — The left lung shows early hemorrhagic patches. In 
 these the central bronchiole and the adjacent alveoli contain streptococci in long 
 chains and in great numbers. There is a fresh exudate of leucocytes with abun- 
 dant red corpuscles but little fibrin. This intensely hemorrhagic exudate with 
 few leucocytes and little fibrin is characteristic of all the patches. 
 
 The right lung shows much edema and a leucocytic exudate in the alveoh. 
 The lymphatics are distended with exudate and here and elsewhere there are 
 myriads of streptococci. In places there are actual abscesses into which the 
 alveolar walls project and end abruptly. These abscesses are loaded with strep- 
 tococci. The bronchial and blood vessel walls are infiltrated with leucocytes 
 and some mononuclear cells. The lower lobe of the right lung shows large 
 
WILLIAM G. MacCALLUM 75 
 
 areas in which the alveolar walls are necrotic and their cavities filled with necrotic 
 material which is loaded with streptococci in long chains. All the surrounding 
 alveoli are packed with red corpuscles with rather few leucocytes and little 
 fibrin. The bronchi in the neighborhood are also full of leucocytes and bacteria, 
 their walls are infiltrated with mononuclears and leucocytes, and markedly thick- 
 ened. The lymphatics are distended with exudate. Streptococci are present 
 everywhere in pure culture and are in long chains of 20 to 30 elements. They 
 have about them a pink-staining material which is ragged and irregular in out- 
 line, like adhering albuminous material. Where there is much fibrin there 
 are no organisms; on the contrary they are especially numerous in the necrotic 
 areas. 
 
 Cultures from right and left lung show Streptococcus hamolyticus . 
 
 The impression gained from this case is that the individual offered no re- 
 sistance to the virulent infection, so that while in the left lung there are patches 
 of lobular pneumonia in its early stages, the right shows extensive areas of necrosis 
 with hemorrhage and little reaction. 
 
 Case 26. — D. C. H., age 21 yrs. Began Jan. 20, 1918, with photophobia, sore 
 throat, fever, and headache. Entered hospital Jan. 25 with conjunctivitis, red- 
 dened throat, Koplik's spots, and red papular rash over entire body. Jan. 30, 
 developed cough and profuse expectoration; rales over entire chest. Temperature 
 98-104° F., pulse 70-150, respiration 15-50. On Feb. 4 and 5 marked dulness 
 over lower left chest. Flatness over left back on Feb. 6. Abundant rales every- 
 where in both lungs. Died Feb. 7, 5.30 a.m. Cultures from sputum showed 
 Streptococcus hcemolyticus in almost pure state. 
 
 Summary of Clinical History. — (Dr. R. Cole.) The signs were those of diffuse 
 pulmonary involvement, especially at the left base, and suggested consolidation 
 rather than fluid. Breath sounds over this area were loud and tubular. Whis- 
 pered voice sounds well transmitted and the tactile fremitus well felt. The per- 
 cussion note over this area was very dull, practically flat. The presence of fluid 
 was suspected, although the signs were not definite. Autopsy Feb. 7, 10.45 a.m. 
 
 Anatomical Diagnosis: Confluent lobular pneumonia. Serofihrinons pleuritis. 
 Atelectasis of lung. Pericardial ecchymoses. 
 
 Left pleural cavity. — Obliterated anteriorly by fresh fibrinous adhesions, but 
 in the posterior part it contains 1,200 cc. of turbid greenish fluid with shreds of 
 fibrin. The pleural surfaces are covered with a thick shaggy exudate of fibrin. 
 Right pleural cavity. — Contains no excess of fluid, but the surfaces have lost 
 their gloss and are roughened by a very thin exudate of fibrin in patches. Left 
 lung (Fig. 41).— There is a thick pleural exudate of fibrin, the underlying pleura 
 being slightly thickened. The lung is flabby and airless except in the anterior 
 margin of the lobes, but on artificial insufflation only the superficial portion 
 of the lower lobe remains collapsed. There are some patches of spongy grey 
 tissue alternating with the generally red lung substance. No areas of actual 
 consoUdation are visible. The bronchi seem relatively little changed, but 
 
76 PNEUMONIA IN ARMY CAMPS 
 
 many of the blood vessels are sheathed in thick yellowish white mantles which 
 shine through the overlying tissue and appear to be due to an infiltration of 
 their adventitia or the distension of the lymphatics in their walls. Bronchial 
 glands are slightly enlarged. Right lung. — Very voluminous and mottled with 
 alternating emphysematous and collapsed areas. In the upper lobe there is an 
 area of homogeneous consolidation with alveoli filled with exudate. In the more 
 posterior part of this lobe there are several small grey foci about 1 mm. in 
 diameter which project slightly. So too in the middle lobe there are several 
 areas of consolidation involving two or three lobules. Elsewhere and through- 
 out the lower lobe there is no consolidation. Pericardium. — There are many 
 minute hemorrhages in the epicardium and in the parietal pericardium. The 
 pericardial sac contains about 50 cc. of fluid which is not turbid but contains 
 floating shreds of fibrin. Pericardial surfaces are glistening. 
 
 Microscopic Examination. — Section through the right lung including the pleura 
 and the margin of one of the sharply outlined areas of consolidation shows that 
 the pleura is covered with fibrin which is thickly sprinkled with streptococci. 
 The interlobular septa are very wide and edematous and enclose a network of 
 fibrin, but this is especially true of the deeper portions and the adventitia of the 
 larger vessels. The bronchi are distinctly but slightly thickened and infiltrated 
 with mononuclear cells. They contain polymorphonuclear leucocytes. The 
 alveolar walls are not thickened or infiltrated. In some areas the alveoli con- 
 tain coagulated fluid with desquamated epithelial cells. In other rather sharply 
 outlined patches they contain packed leucocytes. All these alveoli are found 
 to contain great numbers of streptococci in pairs or short twisted chains. No 
 other bacteria are found. There is practically no fibrin. The streptococci are 
 very numerous in the substance of the pleura and in the lymphatics there, and 
 can be traced through to the fibrinous exudate. 
 
 The uniform consolidation of certain whole lobules is mych like that in lobar 
 pneumonia. Polymorphonuclear leucocytes are densely crowded in the alveoli, 
 but there is little fibrin and few red corpuscles. The alveolar capillaries have a 
 hyaline appearance as though the corpuscles had fused. 
 
 Sections of the left lung show the very thick layer of granulation tissue cov- 
 ered by a thick layer of fibrin which represents the lining of the empyema cavity. 
 From this, greatly widened interlobular septa run into the lung and in them or 
 nearby there are enormous lymphatics distended with a disintegrated fibrino- 
 purulent material loaded with streptococci. 
 
 The bronchial walls are not reaUy much altered in this lung. Some of them 
 are slightly thickened and contain leucocytes and debris. There is a little 
 infiltration of the alveolar walls about blood vessels and bronchi and there are 
 areas of coUapse with hemorrhage and desquamation of epithelium. But the 
 most striking feature is the colossal distension of the lymphatics and it is around 
 them that the infiltration and thickening of the alveolar walls are greatest. 
 
 •Cultures from the lung showed Streptococcus hcemolyticus in both cases. 
 
WILLIAM G. MacCALLUM 77 
 
 Case 55— 0. F. D., age 22 yrs. Had measles at age of 7. On Dec. 27, 1917, 
 developed measles and was in the hospital for 2 weeks. Went on duty Jan. 9, 
 1918, but was very weak. On Jan. 11 was brought to the hospital again with a 
 stitch in his left side and dyspnea. After 9 days was able to walk about, but on 
 Feb. 8 had a chill with severe pain in his left side, vomiting, and cough. Dulness 
 over entire left side with flatness behind and below the middle of the scapula. 
 Tubular breathing at the left apex becoming distant and suppressed at the base. 
 Jaundice and cyanosis. Aspiration of thorax on Feb. 15, but no fluid was ob- 
 tained. Flatness over whole left side with distant tubular breathing. On right 
 side resonance somewhat impaired behind but good anteriorly; breath sounds 
 bronchovesicular with few rales. On Feb. 16, 640 cc. of slightly turbid straw- 
 colored fluid were withdrawn from the left chest and the patient was sent for 
 operation which was performed on Feb. 18 with resection of a rib. Temperature 
 became normal and drainage was good, but from about Feb. 26 to Mar. 7 when 
 the patient died the drainage had decreased, there were signs of septic poisoning, 
 and the temperature was irregular. Cultures from the circulating blood on Feb. 
 
 11 and 15 were negative. The sputum contained Streptococcus hamolyticus and 
 B. influenzce. Fluid aspirated from the chest on Feb. 11 and 16 showed Strep- 
 tococcus hcemolyticus alone. Autopsy Mar. 7, 1918. 
 
 Anatomical Diagnosis: Clinical history of measles. Lobular pneumonia with 
 multiple abscess formation. Empyema {left) . Seropurulent pleuritis. {right) . In- 
 fected infarcts of spleen. 
 
 Left pleural cavity. — In the line of the scapula on the left side there is a wound 
 
 12 cm. long running obliquely along the course of the rib from which a portion 
 has been removed. The cavity is obliterated along the anterior margin of the 
 lung and over its lower portion by old adhesions. The upper part of the 
 pleural cavity is lined by thick yellowish fibrinopurulent exudate. Practically 
 all the fluid exudate has escaped, but there is a pocket containing about 100 
 cc. of thick greenish pus between the diaphragm, the lower mesial surface of 
 the lung, and the pericardium. This communicates with a space between the 
 two lobes. Right pleural cavity. — Contains about 5 cc. of creamy purulent 
 fluid which is spread over the back of the lung and to a less extent anteriorly 
 where the pleura is still shining. The costal and diaphragmatic pleuras are 
 injected and have lost their gloss in the posterior part of the thorax. Left lung 
 {Fig. 42). — The upper lobe is firm except in its anterior lower part which is 
 collapsed. On section it is found that the whole posterior part from the apex 
 down is dense, greyish yellow and moist, but rather thickly studded with 
 patches of opaque pale greenish yellow. At the apex there is one such mass 
 about 2 cm. in diameter and in the lower part there is a great group of them 
 reaching up to the pleura and only partly separated from each other. These 
 patches have softened and partly liquefied foul smelling central portions and 
 hemorrhagic margins. The more anterior part of the lobe shows thickened in- 
 terlobular septa and numerous smaller nodular consolidations. The lower lobe is 
 
78 PNEUMONIA IN ARMY CAMPS 
 
 more flabby and of darker reddish grey color. The interlobular septa are also 
 rather conspicuous and in the lobules there are to be found numerous projecting 
 nodules. There are also several large yellow abscess-like masses. The bronchial 
 glands are large, soft, and grey. Right lung. — The lung is very voluminous 
 (Fig. 43) and the upper lobe easily inflated with air. On section the upper and 
 middle lobes and the anterior portion of the lower lobe are air-containing. The 
 posterior portion of the lower lobe is dark purplish, airless, and fairly firm. There 
 project from its surface a number of opaque firm yellow areas some of which 
 are 3 cm. in diameter. They are partly hidden by the reddened pleura, but in 
 places show through as opaque yellow patches. A similar mass projects from the 
 posterior part of the middle lobe. On section the lower lobe is collapsed and 
 studded throughout, even in the air-containing part, with yellow opaque nodules, 
 the smaller of which seem to have a central lumen. The large ones are quite like 
 those in the upper lobe. Spleen. — Measures 19 by 11 by 5.5 cm. It is quite 
 firm, especially in certain greyish projecting portions which are irregular in 
 outline and surrounded by a red border. On section much of the spleen is 
 greyish in color with distinctly visible trabecule and Malpighian bodies. The 
 splenic pulp is swollen, shining, and velvety. In contrast to this there are 
 irregular patches with ragged outline extending deep into the substance of the 
 organ and bordered by a broad margin of hemorrhage. These patches are dry 
 and opaque with a duU greyish red color. 
 
 Cultures from the heart's blood showed Streptococcus hcemolyticus , and similar 
 Gram-positive cocci were found in abundance in films from the spleen and peri- 
 cardial and pleural fluids, but all autopsy material was grossly contaminated 
 with a Gram-negative spreading baciUus with putrefactive odor. 
 
 Microscopic Examination. — The greatly thickened pleura over the left lung is 
 dense and fibrous and covered with fibrin. The interlobular septa are not es- 
 pecially conspicuous on section. The bronchi although fiUed with purulent exu- 
 date are scarcely thickened or infiltrated. The exudate contains strepto- 
 cocci and Gram-negative bacilli which appear to be influenza bacilli. The alveo- 
 lar walls are nowhere especially thickened nor do they show any extensive 
 desquamation of epitheHum. The alveoli are filled with fluid and leucocytes. 
 There are certain areas in each section which show the especial filling of the 
 alveoli with leucocytes and in these there are whole patches of the central alveoli 
 in which walls and exudate are completely necrotic. In these alveoli streptococci 
 are extraordinarily abundant. They are present in short chains, in tangled 
 masses, or engulfed singly by leucocytes. 
 
 Throughout both lungs the changes appear to be the same. They are defi- 
 nitely areas of lobular pneumonia with large numbers of streptococci causing 
 necrosis and liquefaction, and surrounded by an edematous lung tissue in which 
 the changes characteristic of the interstitial bronchopneumonia do not appear. 
 But there are some areas especially near the thickened pleura where the inter- 
 lobular septa are wider and infiltrated, and the bronchi and blood vessels and 
 
WILLIAM G. MacCALLUM , 79 
 
 even the alveolar walls share in this infiltration. The alveoli in these areas are 
 mostly collapsed, but some are distended with leucocytes and great quantities of 
 streptococci. Most striking is the fact that the lymphatics are enormously dis- 
 tended in many places and filled with fi disintegrated mass of cells and bac- 
 teria. It is evidently frorti these that some of the large necroses begin, although 
 in the collapsed lung around them there are numerous foci in which whole colonies 
 of bacteria are surrounded by necrotic tissue. 
 
 The spleen shows irregular areas of necrosis edged with hemorrhage and studded 
 throughout with veritable colonies of streptococci. The artery supplying one 
 such area is plugged with a softened thrombus which contains the same great 
 masses of organisms. The other organs show no such gross evidence of infection, 
 although there is cloudy swelling of the liver and kidneys. 
 
 Case 56. — F. E., age 40 yrs. Had scarlet fever and measles in early life. 
 For 6 weeks before entrance to hospital had pain in right side whenever he caught 
 cold. On Feb. 7, 1918, had a chill, pain in side, and a temperature of 102° F. 
 Entered the hospital Feb. 8, 1918. There was found dulness over the right 
 lower lobe with distant bronchial breathing. Breathing over left side accentu- 
 ated. Tenderness over abdomen with rigidity of muscles. Temperature 98° F. 
 Leucocytes 24,400. On Feb. 26 the right chest was aspirated and the pleural 
 fluid contained Streptococcus hcemolyticus. Temperature from 100-103° F. for the 
 first 10 days. On Feb^ 19 it fell abruptly to normal and later fluctuated from 
 98 to 101° until Feb. 26. Respiration 40, pulse 100-128. On Feb. 26 the 7th 
 rib was resected under local anesthesia and the right pleural cavity drained. 
 Died Mar. 7, 1918. Autopsy Mar. 8, 1918, 10 a.m. 
 
 Anatomical Diagnosis: Confluent lobular pneumonia with empyema and exten- 
 sion through diaphragm. Pericarditis with effusion. Axillary cellulitis. 
 
 Left pleural cavity. — Free from adhesions. Contains a small amount of fluid, but 
 the surfaces are smooth and glistening although slightly hyperemic posteriorly. 
 Right pleural cavity. — Partly obliterated by very dense fibrous adhesions which 
 enclose a pocket filled with greenish yellow purulent fluid. There is an incision 
 over the 8th rib in the right lateral scapular line which allows the escape of pleural 
 fluid through a rubber drainage tube. The tissue about this wound is very ede- 
 matous and the margins are necrotic. Pericardium. — Contains 100 cc. of yel- 
 low purulent fluid with floating shreds of fibrin. The surfaces are covered with a 
 thick fibrinopurulent exudate. Endocardium normal. Left lung. — Surface is 
 smooth and lung is normally air-containing throughout. Right lung. — The pleura 
 is 3 mm. thick and very dense. It is covered with a layer of fibrin in places. 
 The upper lobe is air-containing. The lower lobe is dense and uniformly grey 
 and consolidated with a few scattered flecks of more hemorrhagic appearance. 
 There is no thickening of the septa or walls of the bronchi. 
 
 Microscopic Examination.: — The left lung is normal. The right is in part 
 edematous with a scattered exudate of polymorphonuclears. The lower lobe, 
 however, shows a compact exudate of these leucocytes filling the alveoli. Septa, 
 
80 PNEUMONIA IN ARMY CAMPS 
 
 bronchial walls, and alveolar walls are delicate and not infiltrated with mono- 
 nuclear cells. 
 
 No cultures were recorded. 
 
 The right lung at its base is adherent to the diaphragm and between them 
 there is a collection of fibrinopurulent exudate. This is seen to extend through 
 the diaphragm so that the dome of the liver is also covered with a localized 
 fibrinopurulent exudate. 
 
 Case 187. — E. S., age 23 yrs. Had German measles on May 2, 1918. On 
 May 6 moist rales throughout both chests, with bronchial breathing in right 
 upper lobe. On May 12 dulness over left upper lobe with fine crepitant rales 
 and high pitched expiration. Friction rub in right axilla. Bronchopneumonia 
 of both lungs on May 8. Sputum on May 8 was purulent, homogeneous, sUghtly 
 blood-tinged, with a few Gram-positive diplococci. Cultures show predominant 
 staphylococcus, few colonies of hemolytic streptococcus. Blood culture was 
 negative May 7, 1918. Died May 13, 1918, at 8.40 p.m. Autopsy May 14, 
 1918, 14 hours after death. 
 
 Anatomical Diagnosis: Cotifluent lobular pneumonia {both upper lobes). Dis- 
 seminated lobular pneumonia with slight interstitial changes. Rupture of rectus 
 abdominis muscle. 
 
 The sheath of the rectus abdominis muscle bulges into the peritoneal cavity 
 on each side at a point just below the umbihcus. On incision it is found that 
 the muscles are torn across and that the ends are retracted leaving a space 
 filled with blood clot and bloody fluid. This rupture is symmetrically placed 
 on the two sides. The ruptured muscle is contracted into a thick belly on 
 each side and there are opaque greyish yellow discolorations seen in the sub- 
 stance of the broken ends. The peritoneal cavity contains no excess of fluid 
 and the surfaces are smooth and ghstening. Left pleural cavity. — The cavity 
 is partly obKterated above by old fibrous adhesions and there are similar ad- 
 hesions between the base of the lung and the diaphragm. The free portion 
 of the pleural cavity contains about 20 cc. of clear fluid and the surfaces are 
 smooth. Right pleural cavity. — Contains very little fluid. The surfaces are 
 smooth except over the upper lobe where there is a thin fibrinous exudate. Left 
 lung {Fig. 44). — The lung is voluminous and in part covered with shreds of old 
 adhesions. The upper lobe is air-containing anteriorly, but firm posteriorly. On 
 section there is found a large area of complete consolidation which is pinkish grey 
 in color and fairly smooth although plugs of exudate can be seen projecting from 
 the alveoli. The bronchi in this area are wide with a dull grey lining, and con- 
 tain a grey purulent exudate. Scattered through the area of consolidation there 
 are irregular patches which are still more prominent and of a lighter yellowish 
 color and more opaque than the rest. These are softened and even partly lique- 
 fied in places. In the anterior air-containing portion there are some nodular 
 consolidations about the branches of the bronchi. The lower lobe is in general 
 air-containing but is rather firm posteriorly. Throughout it there are scattered 
 
WILLIAM G. MacCALLUM i 81 
 
 small peribronchial consolidations such as are seen in the anterior part of the 
 upper lobe. These are more numerous and larger in the posterior part of the 
 lobe. They are not accompanied by any marked hemorrhage. The bronchial 
 glands are much enlarged and are dark greyish red. Right lung. — The lung is 
 large and in general seems to be air-containing. It is found, however, that there 
 is in the posterior middle portion of the upper lobe an area of consolidation about 
 4 cm. in diameter which on section is greyish pink and smooth. Part of the 
 area is yellowish and opaque and appears to be beginning to soften. The anterior 
 part of the lobe is air-containing. The middle lobe is air-containing except for 
 some of the bronchioles which are thickened and filled with exudate and in 
 places surrounded by nodular areas of consolidation. In the lower lobe of this 
 lung there are many bronchioles whose lining epithelium is entirely lost and the 
 surface of the exposed tissue necrotic. These bronchi have greatly thickened 
 walls with extreme hyperemia and infiltration with mononuclear cells. The adja- 
 cent alveoli are generally collapsed, their walls infiltrated with mononuclear 
 cells, and their cavities with blood, fluid, and epithelial ceOs. Pharynx and 
 larynx. — The tonsils are not enlarged. The pharynx is rather pale. The larynx 
 is only slightly reddened and there are no ulcers on the vocal cords or epiglottis. 
 The trachea is slightly reddened. The cervical lymph glands are edematous and 
 greyish red. 
 
 Cultures at autopsy showed Streptococcus hamolyticus in the heart's blood, 
 right and left lungs, and in the bloody fluid between the torn ends of the rectus 
 abdominis muscles. Smears from these localities showed these organisms alone. 
 
 Microscopic Examination. — The lung shows remarkable changes. The pleura 
 is perhaps somewhat thickened over the left lung, but there is no exudate or 
 granulation tissue formation. The interlobular septa are wide and edematous, 
 and contain wide lymphatics which are not thrombosed or at most contain a 
 strand of fibrin. They contain abundant streptococci. The area of consolida- 
 tion in the upper lobe shows no bronchi conspicuous for their thickening, al- 
 though there is a definite mononuclear infiltration of the walls in some cases. 
 The alveolar walls are not infiltrated or thickened. The alveoli are densely 
 packed with polymorphonuclear leucocytes with little fibrin and scarcely any 
 blood (Fig. 45). These leucocytes are fairly loaded with micrococci and there 
 are great quantities of these organisms free between them. It appears as though 
 the leucocytes were inadequate to engulf all of them. 
 
 The alveolar walls are noticeably pale and flattened or thinned out in places. 
 With Weigert's fibrin stain it suddenly becomes evident that the capillaries in 
 many of the alveolar walls are completely obstructed by fibrinous coagula which 
 are not quite homogeneous but fill the whole network of capillaries, at times in 
 such a way as to demonstrate this network as though by a purple injection 
 mass (Fig. 46). Evidently the obstruction to circulation is great and such 
 areas are widely necrotic, there being no nuclei of the alveolar wall left intact 
 enough to stain. Doubtless these are the opaque yellowish patches observed in 
 
82 PNEUMONIA IN ARMY CAMPS 
 
 the consolidated area in the gross inspection. This consoHdation is very dense 
 and extends over a large area in the manner of a lobar or confluent lobular 
 pneumonia. 
 
 In the portion of the lung which is not the seat of a uniform consolidation the 
 bronchi are more definitely thickened by the great hyperemia and new tissue 
 formation which is so often seen. But there is no characteristic surrounding zone 
 of thickening of the alveolar walls with desquamation of the epithelial cells, 
 hemorrhagic organization of the exudate, etc. Instead there are minute patches 
 of lobular consolidation in every respect resembling the large patch in the upper 
 lobe. In the outlying area where there is a great deal of edema this fluid is 
 loaded with bacteria. In places it contains numerous vacuoles which vary 
 greatly in size but are peculiarly surrounded by bacteria which appear to float 
 on the surface of the vacuole. These cavities may be air bubbles from the mix- 
 ing movement of the fluid and the bacteria may swim on their surface in order to 
 be in contact with air, or else their position may be merely an effect of the surface 
 tension of the fluid. The same phenomenon was observed with pneumococci in 
 Case 31. 
 
 There is, therefore, an extraordinarily intense infection with Streptococcus hcemo- 
 lyticus which produces a confluent lobular pneumonia resembling a lobar pneu- 
 monia in places, with only traces of its usual interstitial action. The right lung is 
 similar. Careful search failed to reveal any influenza bacilli. 
 
 Microscopically the rectus muscle shows extensive reduction of muscle fibers 
 to hyahne formless clumps. Where the rupture has occurred there is, of course, 
 much hemorrhage and the separation of fragments of completely necrotic muscle 
 tissue which had already shown the hyaline change in the substance of each 
 fiber. Streptococci are present in quantities in the necrotic ends. The hyahne 
 clumps are found within the sarcolemma sheaths quite far back. They are in- 
 vaded by wandering phagocytic mononuclear cells which can be distinguished 
 from the shoals of sarcolemma nuclei by their more chromatin-rich nucleus. 
 The sarcolemma nuclei are pale with one deeply stained nucleolus. 
 
 Case 192. — J. R. B., age 23 yrs. No history of measles or other predis- 
 posing disease. Began suddenly on May 5, 1918, with a chill and pain in the 
 chest. The diagnosis of lobar pneumonia involving the left lower lobe was 
 made on May 11. Blood culture on Mjay 14 was negative, but the sputum con- 
 tained Staphylococcus aureus and influenza bacilli. Died May 14, 1918. Au- 
 topsy May 15, 1918, 15 hours after death. 
 
 Anatomical Diagnosis: Hemorrhagic bronchopneumonia (bilateral). Ulcera- 
 tive laryngitis. 
 
 Left pleural cavity. — Contains only about 5 cc. of clear fluid. The pleural sur- 
 faces are smooth but flecked with hemorrhage posteriorly. Right pleural 
 cavity. — The cavity contains a little clear fluid. There are a few easily torn 
 adhesions over the apex of the lung. The pleural surfaces are smooth but 
 the lower lobe of the lung is deep blue and covered with areas of hemorrhage. 
 
WILLIAM G. MacCALLUM 83 
 
 Left lung {Fig. 47). — The upper lobe is found to be air-containing throughout, 
 with the exception of very minute foci about the terminal bronchioles which 
 stand out as greyish opaque points. The lower lobe receives a little air in the 
 anterior part. The remainder is deep red and rather nodular lookin'g although 
 the nodules do not stand out very distinct!}'. They appear rather as greyish 
 centers of reddened hemorrhagic areas. Right lung {Fig. 48). — The lung is 
 much more voluminous than the left. The upper lobe is firm in its apical por- 
 tion but otherwise air-containing. The firmness is due to the presence of scarred 
 and pigmented areas at the apex and a little lower on the posterior side. In the 
 lower portion of the lobe posteriorly there are several branching nodular consoli- 
 dations which surround the ends of the bronchi. The middle and lower lobes 
 contain a little air anteriorly but are consolidated posteriorly, the consohdation 
 being produced by greyish nodules surrounded by deep red confluent hemor- 
 rhages. The bronchial lymph nodes are large and greyish red. Pharynx and 
 larynx. — The pharynx and base of the tongue are deeply reddened and the lat- 
 eral walls of the pharynx are covered with an opaque yellow mucoid layer. There 
 is similar congestion of the larynx and trachea, but this does not extend into the 
 esophagus. There are shght erosions of the edges of the epiglottis and a shallow 
 ulceration in the wall of the larynx at the attachment of the vocal cords, but the 
 cords themselves are not ulcerated. 
 
 Cultures at autopsy gave Streptococcus hcsmolyticus from the heart's blood and 
 lungs. 
 
 Microscopic Examination. — The lungs show a fairly uniform process on both 
 sides which is different from any previously described. 
 
 The pleura is densely infiltrated with blood. All crevices and the lymphatics 
 are distended with blood. The interlobular septa are not conspicuous, and 
 where they are found they are in places edematous and infiltrated with mono- 
 nuclear cells and blood. The lymphatics are not prominent but often contain 
 blood and leucocytes. The bronchi are filled with polymorphonuclear leuco- 
 cytes and blood cells. Their walls have usually lost their epithelium and are 
 very hyperemic and edematous but not really thickened or infiltrated with 
 cells. The adjacent alveoli are usually filled with leucocytes. Their walls are 
 not thickened although in places there are leucocytes in their substance. Further 
 from the bronchi the alveoli contain fewer leucocytes and are more and more 
 filled with blood. Indeed, except for the peribronchial filling of the alveoh with 
 leucocytes the whole lung is nearly sohdly filled with red corpuscles with which 
 a few desquamated epithelial cells and leucocytes are mingled. The whole area is 
 one vast hemorrhage. As a rule, few or no bacteria can be found but there 
 are some patches in which streptococci are present in great numbers, sometimes 
 scattered in single chains, sometimes in dense clumps or tangles of chains. Since 
 influenza baciUi were found in the sputum and since the lesion in this lung is so 
 totally unlike that seen in other cases of streptococcus pneumonia the idea 
 suggests itself that it may be due to the influenza bacillus, and search in sec- 
 tions properly stained shows the presence of enormous numbers of minute Gram- 
 
84 PNEUMONIA IN ARMY CAMPS 
 
 negative organisms which may be influenza bacilli, although they often occur in 
 short chains. 
 
 Section of the rectus abdominis (Fig. 49) shows the most extensive hyaline de- 
 generation of the muscle fibers which are reduced to formless clumps of red-stain- 
 ing material still enclosed in the sarcolemma sheath. There are still some intact 
 fibers among the altered ones. The nuclei of the sarcolemma sheaths show no 
 alteration and there is no inflammatory reaction. 
 
 Case 195. — G. M., age 23 yrs. Negro. Began with measles on May 3, 1918, 
 and developed pneumonia which was thought to be a lobar consolidation of the 
 right lower lobe on May 10, 1918. Died May 16. Autopsy May 17, 1918, 11 
 hours after death. 
 
 Anatomical Diagnosis: Clinical history of measles. Disseminated lobular pneu- 
 monia. Empyema {left). 
 
 Left pleural cavity. — Contains 450 cc. of yellowish fluid with flakes of fibrin. 
 The surfaces are covered with a yellowish fibrinous exudate but there are no 
 adhesions. Right pleural cavity. — Contains about 50 cc. of a slightly cloudy 
 fluid. There are on the pleural surface numerous small discrete roughened 
 brownish patches. Left lung. — The upper lobe is air-containing throughout. 
 In the lower lobe there are numerous nodular masses of consolidated tissue 
 which measure 2 by 6 mm. in diameter and surround the bronchioles. These 
 become more numerous in the posterior part of the lobe and are often confluent. 
 Right lung. — There are nodular consolidations scattered throughout all the 
 lobes, becoming more numerous and close set as one passes towards the pos- 
 terior part of the lung. In the upper lobe they are fairly discrete but occupy a 
 large proportion of the lung substance posteriorly. In the middle lobe there is 
 also a larger area of consolidation, a patch 2 cm. in diameter which is firm and 
 grey at the periphery but rather more rose-colored in the center. In the lower 
 lobe the nodules are very numerous especially in the posterior part. The 
 mucosa of the bronchi and trachea is hemorrhagic and deep red. 
 
 No cultures were made at autopsy. 
 
 Microscopic Examination. — The pleura is found to be hyperemic and slightly 
 thickened but still covered by its lining layer of cells. There is a thick layer 
 of fibrin overlying it but there is no sign of organization. The interlobular septa 
 are everywhere wide and edematous. The lymphatics are also wide, and while 
 some of them may be traced along in the septa filled with fluid only, most of them 
 are distended with a compact mass of disintegrated leucocytes, blood, and fibrin 
 with bacteria. Everywhere in the walls of bronchi and blood vessels, in the 
 interlobular septa, and in the pleura the lymphatics are very wide and 
 conspicuous. 
 
 The lung in general is edematous, the alveoli are filled with what appears to 
 be a rather viscid fluid. There are focal areas of consolidation which were recog- 
 nized in the gross and can be seen as such by the unaided eye in the stained sec- 
 tion. It is diflicult to outline these as they shade off into the adjacent tissue in 
 which there is onl}' edema with desquamated epithelial cells. But it is clear that 
 
WILLIAM G. MacCALLUM 85 
 
 there are numerous patches of completely consolidated lung tissue in which 
 every alveolus is filled with polymorphonuclear leucocytes. In and especially 
 about these there is much hemorrhage and then further out the alveoli are found 
 to contain only fibrin with fluid and mononuclear cells which are probably des- 
 quamated epithelium. The bronchi are not at all conspicuous. They contain 
 leucocytes and bacteria. The walls are hyperemia but not infiltrated with cells, 
 nor are the alveolar walls thickened or infiltrated at any point. The most 
 prominent feature in these areas is constituted by the great thrombosed lym- 
 phatics. In places and perhaps especially in these lymphatics the leucocytes 
 are necrotic and disintegrated. In the middle lobe of the right lung the area of 
 uniform infiltration with polymorphonuclears is much greater. There are hya- 
 line thrombi in the capillaries of the alveolar wall and much necrosis of the exu- 
 date and of the walls. The bronchi are but little altered. The consolidation 
 even here is patchy with alternation in the types of exudate. 
 
 In these cases the pleural effusion is quite like that in the preceding 
 groups and it is somewhat surprising to find that a man may survive 
 for 55 days with this lesion extensively developed in association with 
 an old empyema. The gross appearance of the lungs is usually dif- 
 ferent from that found in interstitial bronchopneumonia, since these 
 areas of consolidation are no longer nodular, hard, and prominent, 
 nor especially situated about the branches of the bronchi. Instead, 
 they are very rough, grey, and slightly elevated, often confluent in 
 quite large patches where they resemble closely in their texture the 
 consoHdation of pneumococcal lobar pneumonia. But in many cases 
 they are intensely hemorrhagic and in the central parts dull and 
 opaque. As an example of the first type Case 187 may serve, in 
 which a large area of homogeneous consolidation with granular ex- 
 udate projecting from the alveoli occupies part of the upper lobe, 
 while smaller areas of the same sort are scattered through the lower 
 lobe. In Cases 20 and 192 the areas of consolidation are large and 
 hemorrhagic. 
 
 In all these the participation of the lymphatics is extremely strik- 
 ing. Great beaded canals distended with opaque yellow pus so as to 
 become very conspicuous accompany the blood vessels and bronchi or 
 run in the line of the interlobular septa to the pleural surface. These 
 stand out especially in Cases 20 and 26 and can be readily traced to 
 their connection with the network in the pleura which is similarly 
 prominent and distended with pus. 
 
86 PNEUMONIA IN ARMY CAMPS 
 
 In Case 55 extensive areas of necrosis occur in which the lung sub- 
 stance is converted into a soft yellow opaque material. These areas 
 look like abscesses as they project under the pleura and possibly they 
 should be so called, but they are really pretty firm opaque necrotic 
 patches of consolidated lung swarming with streptococci but still 
 composed of coagulated tissue and not of pus. There is no real dis- 
 tinction except perhaps in the lack of an intense leucocytic invasion 
 to reduce this necrotic material quickly to a liquid state. In other 
 cases it has been seen that such areas may be discharged through a 
 bronchus the walls of which are interrupted on entrance into the ne- 
 crotic patch. This leaves a cavity which may or may not communi- 
 cate with the pleural cavity. In none of our cases had this actually 
 occurred, but it seems that this is the explanation of the formation of 
 the pleurobronchial fistulse which are encountered by many surgeons 
 in treating the late empyema cases. 
 
 Microscopically the lesions just mentioned are the outcome of the 
 filling of alveoli with streptococci and an exudate of leucocytes and 
 fibrin. The streptococci are extremely abundant throughout this 
 exudate. In Case 187 in which the consohdation is almost lobar in 
 appearance the capillaries of the alveolar walls are widely thrombosed 
 with hyaline strands of fibrin which completely occlude them. The 
 exudate and even the tissue of the lung becomes necrotic under these 
 conditions. 
 
 In the more hemorrhagic consolidation such as is seen in Case 20, 
 great stretches of lung substance simply become necrotic and filled 
 with blood without any adequate infiltration of leucocytes. In such 
 places the streptococci in long chains form a tangled matted growth 
 as though they were growing in the most favorable culture medium. 
 In the outlying parts of the lung about these places there are alveoli 
 filled with leucocytes and fibrin but the destructive process seems to 
 have been too intense and rapid to allow the institution of a proper 
 reaction. The lymphatics distended with leucocytes, fibrin, and 
 myriads of streptococci form enormous objects in the microscopic 
 field. 
 
 The lesion then in all these cases is produced by the streptococcus; 
 it is the simplest inflammatory reaction to the invasion of great num- 
 bers of streptococci and often even this reaction fails, so that with 
 
WILLIAM G. MacCALLUM 87 
 
 great extravasation of blood the whole invaded area becomes necrotic 
 and a good soil for unlimited multiplication of the organisms. It 
 represents the most passive attitude of the body in which resistance 
 is at its lowest. 
 
 The Changes in Other Parts of the Respiratory Tract in Streptococcal 
 
 Pneumonia. 
 
 No distinction is practicable between the groups of cases just con- 
 sidered in so far as the lesions of the rest of the respiratory tract are 
 concerned. The changes in the lung proper have been described 
 and the forms of pleurisy will be analyzed later. There remain the 
 bronchial glands, the larger bronchi and trachea, the larynx, and the 
 upper air passages. 
 
 The bronchial lymph glands are always somewhat enlarged al- 
 though not so greatly as in some other affections of the lungs. They 
 are soft, edematous, and greyish red except when deeply pigmented. 
 I have encountered no abscesses in these glands. The cervical and 
 peritracheal glands are often similarly affected. Microscopically 
 they show in each case a considerable increase in the cells of the 
 lymph cords and islands, but it is in the sinuses that the change is 
 most marked. These are very wide and are packed with cells, chiefly 
 large and small mononuclear wandering cells which have probably 
 been swept into these sinuses from the lymphatics of the lungs since 
 they are of the type seen there. They are to some extent phagocytic, 
 loading themselves with the debris of other cells. There is no evi- 
 dence that they are derived from the endothelium of the sinuses which 
 is intact. Among these there are quantities of streptococci often 
 single or in pairs, often in tangled masses. 
 
 The large bronchi and trachea are deeply reddened, covered with 
 purulent exudate, and occasionally with a pseudomembrane which is 
 generally limited to the bronchi. Streptococci are found abundantly 
 strewn along the surface of the mucosa. 
 
 In the acuter cases and especially in those in which the disease is 
 associated with measles there is aphonia with corresponding changes 
 in the larynx. These changes, which are found in Cases 165, 178, 
 184, 192, 194, 180, and others, consist in an intense reddening of 
 
'88 PNEUMONIA IN ARMY CAMPS 
 
 the mucosa often with some edema. Most striking, however, is* the 
 ulceration which commonly affects the vocal cords and causes a 
 deep loss of substance along their whole edges. Microscopically 
 it is found that the epithehum and underlying elastic tissue is 
 necrotic or has been swept away completely leaving the base of the 
 ulcer thickly strewn with streptococci. Streptococci are found in 
 crevices of the neighboring tissue and in folds of the mucosa nearby. 
 Similar ulcerations occur on the epiglottis, on the arytenoepiglottic 
 folds, in the pyriform sinuses, and elsewhere, in the walls of the 
 pharynx and larynx. In Case 165 there was a marked swelUng of 
 the arytenoepiglottic folds and of the epiglottis with only a shallow 
 superficial ulceration, but all the swollen tissue was packed with 
 streptococci and a diffuse inflammatory exudate. Most of the other 
 cases, however, showed no especial alteration in the larynx. The 
 walls of the pharynx are generally deeply congested and in a few in- 
 stances there was a superficial ulceration of the uvula and of the 
 pillars of the fauces. The tonsils are not much enlarged or altered in 
 appearance, and although streptococci can be found in clumps in the 
 depths of the crypts there is no especial reaction of an inflammatory 
 character about them. We were, of course, concerned with the idea 
 that the tonsils might harbor the streptococci and in this way play 
 an important part in the development of the disease, but it is not 
 even certain that the clumps of streptococci which often have a 
 radial marginal arrangement are of the same character as those which 
 produce the pneumonia. At any rate the impression received was 
 that the tonsils are passive in this process. The hemolytic strepto- 
 coccus from outside seems to sweep past them through the pharynx, 
 the larynx, and trachea into the bronchi. At most they fail in their 
 function as guards, and this may be said too of the lingual and other 
 adenoid tissue which becomes sHghtly swollen. 
 
 The condition of infection of the accessory sinuses which com- 
 municate with the nasal cavity and of the nasal mucosa itself is un- 
 known to me as there was no opportunity to investigate them. It 
 seems, however, that they may be the first to become infected and 
 they should be studied. It is evident that inflammation follows the 
 extension of infection up the Eustachian tube to the middle ear, for 
 otitis media is by no means uncommon as a complication (Cases 205, 
 21,181). 
 
WILLIAM G. MacCALLXTM 89 
 
 Lesions in Other Organs. 
 
 The channel of infection of the pericardium is not clearly decided. 
 It seems probable that infection must take place by extension from 
 the pleura although this is difficult to demonstrate, and it is puzzhng 
 to find so many cases of intense pleural infection without pericarditis. 
 
 In the whole series of 60 cases there were ten in which there was a 
 definite pericarditis. Of these, two, Nos. 19 and 186, were associated 
 with lobar pneumonia caused by the pneumococcus; two others, Nos. 
 36 and 46, occurred in cases in which the pneumococcus and strepto- 
 coccus were both present, and the remaining six were in cases of 
 streptococcus infection, although three of these at least. Cases 56, 57, 
 and 176, were associated with very old empyema in which the bac- 
 terial flora was no longer uncontaminated. There are no sharply 
 distinctive features in the streptococcus pericarditis, although there 
 seems to be a tendency to great thickening of the pericardial tissues 
 and the formation of obliterating adhesions. In one. Case 203, the 
 pericardial sac was enormously enlarged and thickened and con- 
 tained at autopsy 1,000 cc. of thick pus, although it had been aspir- 
 ated by the surgeon some days before. The others presented a thick 
 turbid purulent fluid with shaggy fibrinous exudate on the pericardial 
 surfaces. There were several other cases in which minute hemor- 
 rhages and a slightly cloudy and somewhat increased fluid attracted 
 attention to the pericardium, but in these the pericardial surfaces 
 were still glossy. 
 
 Endocarditis was present in one case, No. 45, of lobar pneumonia, 
 and the pneumococcus was isolated from the vegetations. One case, 
 No. 24, showed a lobular pneumonia with some of the features of an 
 interstitial bronchopneumonia in which there was acute endocarditis, 
 but the body was partly decomposed, and although streptococci were 
 present in smears the exact nature of the case is not clear. In none of 
 the more definite instances of streptococcal pneumonia was there 
 endocarditis. 
 
 The spleen in the cases of streptococcal pneumonia was sometimes 
 slightly enlarged and occasionally rather soft. On the whole, however, 
 it showed no definite change from normal, and microscopic exami- 
 nation failed to reveal any marked alteration of any part of its 
 
90 PNEUMONIA IN ARMY CAMPS 
 
 structure. In one case only, No. 55, which was a case of lobular 
 pneumonia with large areas of necrosis or abscess formation and an 
 empyema of 55 days standing, were there infarct-like infected areas 
 scattered through the substance. These on microscopic examination 
 showed the presence of whole colonies of streptococci and Gram- 
 negative bacilli lying in the middle of necrotic and disintegrated areas. 
 
 The liver in most instances showed a moderate cloudy swelling, but 
 otherwise no departure from the normal. In one case only, No. 16, 
 were there fresh midzonal necroses throughout the organ. 
 
 In general the kidneys were normal in appearance except for a 
 slight cloudiness of the cortex which appeared in microscopic section 
 as a slight swelling of the epithelial cells of the convoluted tubules. 
 But in four cases, Nos. 35, 36, 171, and 188, there was an acute ne- 
 phritis with petechial hemorrhages and swelling and some opacity of 
 the cortex. Microscopically these cases showed glomerular lesions 
 characterized by hyaline thrombosis of the capillaries with hemor- 
 rhage and exudation of leucocytes into the Bowman's capsules and 
 tubules and the accumulation of leucocytes and wandering cells in 
 the interstices of the tissue. Epithelial degeneration was present in 
 only moderate degree. But of these four cases two, Nos. 36 and 188, 
 were essentially pneumococcus infections and were really cases of 
 lobar pneumonia. Acute nephritis therefore occurred in only two of 
 the cases of streptococcal infection and cannot be regarded as a char- 
 acteristic accompaniment of this infection but rather as an accidental 
 occurrence. . 
 
 The peritoneal cavity was infected, however, in several cases, so 
 that acute peritonitis seemed to be a not infrequent accompaniment 
 of the streptococcal pneumonia. 
 
 In this series five cases in all showed an acute peritonitis and of 
 these one, No. 51, was a case of pneumococcal pneumonia with pneu- 
 mococci in the peritoneal exudate. In the others, Nos. 35, 165, 176, 
 and 194, the peritoneal exudate contained the streptococci. They 
 were all rather old cases of streptococcal pneumonia with empyema. 
 No origin could be found for the peritoneal infection in the abdom- 
 inal organs, and it may be that extension of the infection occurred 
 through the lymphatics of the diaphragm. Indeed it seemed possible 
 to trace this directly in Case 194. 
 
WILLIAM G. MacCALLUM 91 
 
 In Case 56 there was a gross extension of the infection through the 
 diaphragm so that an abscess-like accumulation of pus on the pleural 
 surface communicated freely with a similar enclosed pocket on the 
 upper surface of the liver. 
 
 The testes show in nearly all these cases an extraordinary change 
 which is especially striking in the streptococcal infections, although 
 occurring sometimes in the pneumococcal infection and failing to 
 appear in some of the streptococcal ones. It appears to consist in a 
 cessation of spermatogenesis which has probably come about through 
 a stoppage of mitosis at an early stage. In most of the cases of 
 streptococcal infection spermatozoa are not to be found in the tubules 
 of the testis, although a few may persist in the seminal vesicles em- 
 bedded in the viscous fluid which is found there. Not only are the 
 spermatozoa absent, but in many cases one looks in vain for sperma- 
 tids or spermatocytes. The spermatogonia are always present, and 
 the Sertoli cells become very conspicuous, but with only these types 
 of cells left the tubule is reduced to an extremely simple structure. 
 
 The interstitial tissue is less altered although frequently greatly 
 increased in bulk. Leydig's cells are generally unchanged. It is 
 possible that older changes, such as the complete conversion of the 
 tubules into hyaline strands, and even the great thickening of the 
 interstitial tissue may be the remains of some earher injury such as 
 may have resulted from mumps. But the cessation of spermato- 
 genesis is so constant that it must be ascribed to the present disease. 
 Among the cases of pneumonia caused by the pneumococcus two or 
 three showed normal tubules, but the rest exhibited various stages 
 in the same process leading to the interruption of formation of 
 spermatozoa. 
 
 This matter has been discussed by Cordes, who found this condition 
 after many acute infections. Details of the present material need 
 not be given here. 
 
 Bone marrow taken from the femur in a great number of these 
 cases showed uniformly an increase in the cell content, depending 
 especially upon an increase in the myelocytes. It was not different 
 from that observed in many other acute infections accompanied by 
 leucocytosis. 
 
92 PNEUMONIA IN ARMY CAMPS 
 
 In Cases 187 and 205 there was found a symmetrical rupture of the 
 two sides of the rectus abdominis in its lower third. The separation 
 of these torn ends was accompanied by the production of a consider- 
 able hematoma such as is often seen in the same position in typhoid 
 fever — the so called Zenker's degeneration of the muscle. Study of 
 these and other rectus abdominis muscles shows that there is a most 
 extensive hyaUne degeneration of the fibers which are broken into 
 irregular masses of glassy material with no trace of the former stria- 
 tions. These become surrounded by the concentrated nuclei of the 
 sarcolemma sheath and new cellular connective tissue springs up be- 
 tween them. Before long such weakened muscles tear with cough- 
 ing or some other strain and the hemorrhage occurs. In Case 187 the 
 streptococcus was found in the bloody fluid, but in the other there 
 were no bacteria. In Case 192 there was no such rupture, but al- 
 though the rectus muscle looked normal it showed microscopically a 
 very extensive degeneration of its fibers (Fig. 49). Muscle taken 
 from the corresponding point in several other cases failed, however, to 
 show any degeneration. It seems probable that this is not the direct 
 effect of infection, but that it is caused by some toxic process after 
 which bacteria may lodge on the necrotic material. 
 
 In another case, No. 45, in which the pneumococcus was found in 
 the pneumonic lesion there were symmetrically placed abscesses in 
 the same position occupying most of the substance of the lower third 
 of the rectus abdominis on each side. In these the pnemnococcus 
 was found. Several other cases of this kind were observed at Fort 
 Worth, Texas. 
 
 The lodgement of streptococci in other parts of the body, such as 
 the bones, joints, and muscles, appears not to be very common. 
 
 In Case 176 in which there was an old empyema there was found 
 an extensive abscess among the muscles of the neck reaching upward 
 toward the left ear and downward past the dome of the pleura into the 
 muscles between the scapula and the vertebral column. How the 
 infection reached this region is not clear. The pleural cavity was not 
 in communication with the abscess, and the shoulder joint was normal 
 although surrounded. It seemed possible that it might have been 
 due to extension from the pleura, but this was not proven. In no 
 other case was there any such area of infection away from the res- 
 
WILLIAM G. MacCALLITM 93 
 
 piratory organs themselves. Nevertheless I have heard from various 
 surgeons of the occurrence of abscesses in the muscles and subcuta- 
 neous tissues in different localities. Although joint infections have 
 been described we met with none in these cases. 
 
 The question of the existence of a streptococcal septicemia is much 
 discussed and there are differences of opinion on the point. We 
 have made in all about 100 blood cultures^ from the circulating blood 
 taken from the arm vein at various times before death with the usual 
 technique of adding the blood to sterile broth, etc., but none of these 
 cultures gave a positive result except when they were taken just 
 before death. Even then there were very few positive results and 
 the contrast between this organism and the pneumococcus is made 
 more striking by the fact that in the cases in which lobar pneumonia 
 is found combined with interstitial bronchopneumonia the pneumo- 
 coccus has been isolated from the circulating blood, but not the strep- 
 tococcus. Of course after death the heart's blood gives invariably a 
 culture of the streptococcus. It seems that the conditions produced 
 by the streptococcus are once more comparable with those produced 
 by the tubercle bacillus, because in chronic phthisis we do not find the 
 tubercle bacilli circulating in the blood as must be the case in gener- 
 alized miliary tuberculosis; nevertheless scattered tubercles in all the 
 organs attest the fact that at least a few tubercle bacilli are able to 
 enter the blood stream. So with the hemolytic streptococcus. Its 
 distribution is chiefly local in the respiratory tract, but enough strep- 
 tococci may from time to time enter the blood stream to give rise to 
 an occasional abscess. 
 
 4. Lobar Pneumonia. 
 
 Case 18. — J. P. W., age 30 yrs. Previous history negative. Developed cold 
 and hoarseness Jan. 14, 1918. Entered hospital Jan. 26, with nausea and vomit- 
 ing, chill, fever, and cough. Pain in back and right shoulder. Dtilness, prolonged 
 expiration, increased vocal fremitus, and crepitant rales over lower left back. 
 Leucocytes 19,000. Temperature 104-101° F., pulse 100-150, respiration 26-50. 
 Developed signs of consolidation at right base Feb. 1 and died Feb. 3. Autopsy 
 Feb. 3. 
 
 ^ These cultures were made by the Commission in Texas, and at Camp Dodge 
 by Captain Sellards and Lieutenant Toomey. 
 
94 PNEUMONIA IN ARMY CAMPS 
 
 Anatomical Diagnosis: Lobar pneumonia (left lung) with fibrinous pleuritis. 
 
 Left pleural cavity. — Obliterated by fresh fibrinous adhesions anteriorly, but in 
 the posterior part there are 200 cc. of turbid fluid. The lung is covered with an 
 edematous layer of fibrin measuring 2 cm. in thickness in places. Right pleural 
 cavity. — Contains no fluid, surfaces glistening. Left lung. — The upper lobe is air- 
 containing anteriorly, but in its posterior portion is completely and uniformly 
 consohdated. In the anterior portion there is also a patchy consolidation with a 
 few masses of yellowish fibrinous material embedded in the substance of the 
 lung. In other places the walls of the vessels and bronchi are edematous. In 
 the lower lobe the consolidation is uniform and of a greyish red color. It is 
 distinctly produced by the fiUing of the alveoli with exudate. Right lung. — With 
 the exception of the posterior portions of the upper and lower lobes which are 
 atelectatic and a small area, of consolidation in the upper lobe, the lung is air- 
 containing. The bronchi are normal in appearance. 
 
 Microscopic Examination. — The left lung shows a loose thick layer of fibrin upon 
 its surface. The pleura itself is slightly thickened by hyperemia, edema, infil- 
 tration of leucocytes, and some new formation of connective tissue cells. The 
 layer of cells lining the pleural cavity is still visible, however, and no organization 
 of the overlying fibrin has occurred. Numerous pneumococci can be seen scat- 
 tered through the layer of fibrin and usually enclosed in phagocytic leucocytes. 
 The same condition is found in the interlobular space where the surfaces are 
 bound together by fibrin, but there organization appears to have begun. 
 
 The bronchi contain an exudate of leucocytes and red corpuscles. The alveoli 
 are uniformly filled with an exudate of red corpuscles, leucocytes, and fibrin. 
 Pneumococci are seen scattered diffusely in the exudate, both in the bronchi 
 and alveoli. It is clear that the fibrin is more conspicuous in the alveoli adjoin- 
 ing the interlobular septa, but organisms are not obviously more abundant in 
 the more central parts adjacent to the bronchi. The alveolar walls are distinctly 
 infiltrated with leucocytes and occasional mononuclear cells. So too are the 
 bronchial walls and walls of blood vessels, as well as the interlobular septa. This 
 is not enough to make them prominent, however, and in general all these struc- 
 tures are but slightly thickened. The lymphatics in the bronchial walls, adven- 
 titia of blood vessels, interlobular septa, and pleura are greatly distended with a 
 network of fibrin entangling red corpuscles and leucocj'tes. In these pneumococci 
 are found. Some of these lymphatics are enormous and readily visible to the 
 naked eye as yellow beaded strands in the consohdated lung. 
 
 The bronchial lymph glands are extremely hyperemic and the afferent lymph 
 sinuses are greatly distended with red corpuscles and large phagocytic mono- 
 nuclear cells. Pneumococci are abundant there, but there are few in the remainder 
 of the gland. 
 
 Cultures showed Pneumococcus Type IV from the heart's blood and both 
 lungs. 
 
WILLIAM G. MacCALLUM 95 
 
 Case 19. — B. N., age 27 yrs. Previous history negative. Taken sick suddenly 
 Jan. 29, 1918, with vomiting and pain in the right liypochondrium. Entered 
 hospital Jan. 30, and on Jan. 31 complained of acute pain in right chest. Dulness 
 over upper lobe of right lung. Leucocytes 18,800. Temperature 101-103° F., 
 fallitig to 99° before death. Pulse 90-130. Died Feb. 3. Autopsy Feb. 4. 
 
 Anatomical Diagnosis: Lobar pneumonia {right upper lobe) with fibrinopurulent 
 pleurisy. Fibrinopurulent pericarditis with abundant effusion. 
 
 Left pleural cavity. — Contains a little brown fluid. Surfaces are covered over 
 the lower lobe by a thin fibrinous exudate. The lung is adherent at the apex 
 posterioWy. Right pleural cavity. — The anterior portion of the lung is glued to 
 the parietal pleura and to the pericardial sac. Between the pericardium and the 
 mesial surface of the lung there is an encapsulated cavity containing about 100 
 cc. of fibrinopurulent exudate. The posterior part of the pleural cavity is filled 
 with similar exudate which bathes the lower lobe. Its surface is covered with a 
 thick layer of fibrinous exudate. The upper lobe is adherent by fresh fibrinous 
 adhesions to the costal pleura. Left lung. — Air-containing throughout. The 
 bronchial glands are soft and pigmented but not enlarged. Bronchi are pale and 
 contain sticky mucus. Right lung. — The upper lobe is uniformly consolidated, 
 the cut surface showing a greyish red exudate which fills all the alveoli. The 
 interlobular septa are prominent, the bronchi distended with opaque yellow 
 exudate. The middle and lower lobes are almost entirely collapsed except in 
 their anterior margins. There is no consolidation. Pericardium. — The peri- 
 cardial sac contains 550 cc. of a thick greenish turbid fluid with floating shreds 
 of fibrin. The surfaces are thickly covered with yellowish fibrinous exudate. 
 
 Microscopic Examination. — The consolidated part of the right lung shows a 
 thin pleura with a covering of fibrin which is not organized; the lining cells of the 
 pleura are still visible. The interlobular septa are widened and edematous, and 
 a network of fibrin extends throughout their length. Numerous pneumococci 
 are found scattered through the fibrinous exudate on the pleura and many are 
 enclosed in phagocytes. The bronchi contain a purulent exudate. The walls 
 are slightly thickened and infiltrated with mononuclear cells. The alveolar walls 
 are in general thin but some are infiltrated with leucocytes, and in the neighborhood 
 of the large vessels, broad interlobular septa, and pleura there is a thickening of 
 the alveolar walls by mononuclear infiltration. 
 
 In the alveoli the exudate, composed of red corpuscles, leucocytes, and fibrin, 
 is loaded with pneumococci which are uniformly scattered. Some of them are in 
 phagocytes. Even the alveolar walls are occasionally invaded by them. The 
 lymphatics are everywhere greatly distended with a clotted exudate of leucocytes 
 and mononuclears together with large quantities of pneumococci. 
 
 There is a fresh pericarditis. The lining layer of cells is still complete and the 
 fibrinous exudate is alternately compact and loose. 
 
 Cultures from the lung show Pneumococcus Type II. 
 
96 PNEtJMo^rIA in army camps 
 
 Case 25. — F. G. W., age 24 yrs. Previous history negative. Measles and 
 mumps at 6 years. On Jan. 30, 1918, had a chill followed by fever and pain in 
 right side. Entered hospital Feb. 1, expectorating rusty sputum. Dulness 
 and tubular breathing over both sides posteriorly. Extreme cyanosis. Leuco- 
 cytes 19,800. Temperature 99-103° F., pulse 110-140, respiration 25-35. Died 
 Feb. 6. On account of the coarse bubbhng rales it was suggested that the pneu- 
 monia was in the stage of resolution. Cultures from sputum and circulating 
 blood gave Pneumococcus Type II. Autopsy Feb. 6. 
 
 Anatomical Diagnosis: Lobar pneumonia (bilateraf). Fibrinous pleuritis. 
 
 Lejt pleural cavity. — Contains no excess of fluid. There are old adhesions over 
 the posterior portion of the lung. Right pleural cavity. — Surfaces are glued 
 together by fibrin and there is no fluid. Left lung. — The upper lobe is soft and 
 cushiony and, although much pigmented, is air-containing throughout except for 
 small areas of consolidation in the lowermost portion. The lower lobe shows ex- 
 tensive though somewhat patchy consolidation in which the individual alveoli are 
 seen tocontain plugs of exudate. Right lung. — The anterior part of the upper lobe 
 is air-containing. The posterior part of the upper lobe, the whole of the middle 
 lobe, and all of the lower lobe except the lowermost margin are consoHdated. 
 This consolidated tissue on section is smooth and grey and uniform in appear- 
 ance; the alveoli are not easily made out to contain individual plugs. 
 
 Microscopic Examination. — The right lung shows an intraalveolar consolida- 
 tion which stops sharply at the limit of the lobe. The interlobar cleft is filled 
 with fibrin entangling a few leucocytes. The pleural cells are well preserved 
 and on the pleural surface covered with a thin layer of fibrin which is not organ- 
 ized. The bronchi show no modification of their walls except a subepithelial 
 accumulation of polymorphonuclear leucocytes. The lumen of each bronchus 
 is filled with leucocytes. The alveolar walls are distinctly thickened (Fig. 50) 
 through the accumulation of polymorphonuclear leucocytes between the capil- 
 laries and within the substance of the alveolar wall in such a way as to lift up 
 from the capillaries into rounded eminences what seems to be a very thin struc- 
 tureless membrane upon which the alveolar epithehum lies. The thickening is 
 thus very uneven and the alveolar surface of one of the walls presents a series 
 of mammillations. In general the epithelial cells are greatly swollen and most 
 of them are desquamated. The alveoli contain a loosely attached and rather 
 shrunken network of fibrin with granular looking leucocytes and very numerous 
 large round mononuclear cells which are active phagocytes and are stuffed with 
 fragments of leucocytes. Pneumococci have been found by Weigert's stain in 
 small numbers. There is much pigment in the lung, and interlobular septa as 
 well as vessel and bronchial walls are loaded with it. Other portions of the lung 
 where there is no consolidation are normal except for this. 
 
 Cultures from the lung showed Pneumococcus Type II. 
 
 Case 33. — D. K., age 21 yrs. Began about Jan. 5 with a cold and chilly feel- 
 ing after exposure to rain. Entered hospital Jan. 9, 1918, with fever, headache. 
 
WILLIAM G. MacCALLUM '97 
 
 cough, and a macular eruption which was diagnosed measles. Jan. 11, pain in 
 both Tears. Drums incised and pus discharged. Jan. 20, much cough with r^les 
 over whole chest. Feb. 1, dulness in both lower lobes. Feb. 5, leucocytes 8,600. 
 Temperature very irregular, varying daily from 97-103° F., pulse 80-110. On 
 Feb. 7 rash had disappeared, throat not reddened. Dulness merging into flat- 
 ness over left lower lobe with tubular breathing in that area. Elsewhere indefinite. 
 Thoracentesis on the left side below the angle of the scapula gave 60 cc. of bloody 
 fluid which contained Gram-positive insoluble cocci apparently streptococci. 
 The sputum contained similar cocci and influenza bacillus. Blood culture on this 
 day gave Pneumococcus Type IV. Feb. 8, patient very ill; temperature 104°. 
 Lungs resonant anteriorly with large rales. Died Feb. 10, at 4 a.m. Autopsy 
 Feb. 10, 10 a.m. 
 
 Anatomical Diagnosis: Bilateral lobar pneumonia. 
 
 Left pleural cavity. — Contains 800 cc. of greenish yellow fluid with shreds of 
 fibrin. The pleural surfaces are shaggy and covered with a fine honey-combed 
 layer of fibrinous exudate. Right pleural cavity. — Contains no excess of fluid; 
 there are some fresh adhesions over the posterior surface of the lung which are 
 easily broken through. There are also interlobar adhesions which are rather 
 lax. Left lung. — The upper lobe is in general air-containing, although in its 
 lower part there are a few yellowish opaque patches surrounded by hyperemic 
 zones. The lower lobe is quite uniformly consolidated, the alveolar exudate 
 projecting as minute granules which give the cut surface a reddish grey color. 
 The septa are not conspicuous. The bronchi are somewhat reddened, the 
 bronchial glands enlarged. Right lung. — The anterior portions of all the lobes 
 are distended with air. The upper lobe is air-containing except in its lower 
 portion where there is a patch of uniform consolidation. There are pretty dense 
 interlobar adhesions. The middle lobe contains only a few small foci of con- 
 solidation which are grey and prominent. The lower lobe shows a rather peculiar 
 distribution of the consolidation. There is a wedge-shaped area extending up- 
 ward and backward from the hilum and about 3 cm. in width at its base at 
 the pleura. There is also a large irregular area measuring about 10 by 5 
 cm. which extends through most of the lower and posterior part of the lobe. 
 These are greyish red and uniformly consolidated. Between these and below the 
 lower one there are air-containing portions of the lung. The bronchi are only 
 slightly reddened and not thickened or prominent. The interlobular septa are 
 rather conspicuous. The lymph glands at the hilum are large and soft. Other 
 organs show no especial alteration. 
 
 The blood post mortem gave Streptococcus hamolyticus and the influenza bacillus. 
 Cultures from both lungs gave Streptococcus hamolyticus alone. 
 
 Microscopic Examination. — The consohdated tissue from the left lower lobe 
 shows a typical lobar pneumonia. The pleura is covered with a thin layer of fibrin 
 with numerous leucocytes and innumerable cocci in pairs. The pleural membrane 
 itself is hyperemic but not especially thickened or infiltrated and there is no 
 
98 PNEUMONIA IN ARMY CAMPS 
 
 trace of organization of the overlying fibrin. The interlobar spaces present the 
 same appearance. The bronchi contain a purulent exudate with enormous 
 numbers of cocci in pairs. There are also great numbers of influenza bacilli. 
 There is a slight infiltration of their walls with leucocytes and a few mono- 
 nuclear cells, but this is relatively inconspicuous. The alveolar walls are normal 
 in thickness and are nowhere infiltrated with cells. The capillaries seem to be 
 on the whole rather empty and compressed. The alveoli are closely packed 
 with leucocytes. Those nearest the atria and bronchioles are especially full 
 of these leucocytes, while in the peripheral parts of the lobule fibrin occupies a 
 part of the space. The leucocytes are disintegrating and although in most places 
 the nuclei are well preserved the cell outhne is ragged or indistinct. Red cor- 
 puscles are scarcely seen. The leucocytes have acted as phagocytes and many 
 of them appear as rounded packets of micrococci. The bacteria are numerous 
 especially in the alveoli which are centrally placed and free of fibrin. These 
 are rather elongated cocci in pairs arranged stiffly and suggesting pneumococci 
 rather than streptococci. Their distribution is that of pneimiococci also. The 
 interlobar septa are rather wide and are infiltrated with fluid and fibrin. The 
 blood vessels and lymphatics which run in these septa contain leucocytes and 
 fibrin with many organisms. The bronchial glands show a great collection of 
 large phagocytic cells in their sinuses which are much widened to accommodate 
 them. 
 
 Other portions of the lung aside from the consolidated area show, especially 
 in the lower lobe of the right side, a great deal of edema. The bronchi are in 
 most places fiUed with leucocytes and there is a slight infiltration of their walls. 
 In the alveoli which contain fluid there are great numbers of cocci. These are 
 commonly collected about minute rounded spaces so that they lie in the fluid on 
 the surface of these bubble-Hke spaces. Such spaces are no larger than a leuco- 
 cyte and often form a network in the coagulated fluid contents of the alveolus. 
 In most places the same stifif arrangement of the cocci in pairs is seen, but in 
 some alveoli there are bacteria of different form. There are minute round cocci 
 arranged in long wavy or twisted chains. These are evidently streptococci and 
 distinguishable by their morphology even in the tissue. They are not abundant 
 and the pneumococci seem well preserved so that it is remarkable that strepto- 
 cocci alone were recovered in cultures from the lung. Other organs show no 
 especial alteration. 
 
 Case 36. — J. W., age 29 yrs. No history of measles. Entered hospital Jan. 
 19, 1918, complaining of dizziness and headache, pain in left side of chest, cough, 
 and expectoration of blood-streaked sputum. Throat negative. Signs of con- 
 solidation in lower lobes of both lungs. Blood culture negative. Leucocytes 
 40,800. Urine shows faint trace of albumin, otherwise negative. Temperature 
 102-105° F., gradually falling to 98° at time of death. Pulse about 100, respira- 
 tion 30-40. Sputum showed Pneumococcus Type I. Was given antipneumo- 
 coccus serum Jan. 19. Feb. 1, feet became edematous. Insomnia on account of 
 
WILLIAM G. MacCALLUM 99 
 
 dyspnea-. Urine shows albumin, pus cells, blood, and granular casts. Died Feb. 
 12, 1918. Autopsy Feb. 12, 1918. 
 
 Anatomical Diagnosis: Lobar pneumonia with encapsulated-^mpyema (left). Sero- 
 fibrinous pleuritis {right). Subacute pericarditis. Acute nephritis. 
 
 Left pleural cavity. — Contains a considerable quantity of thick greenish yellow 
 pus which is encapsulated in several distinct and non-communicating pockets. The 
 largest of these pockets containing about 300 cc. of pus lies between the anterior 
 border of the lower lobe and the pericardium. The other pockets are between the 
 lower lobe and the lateral chest wall. Posterior to the upper lobe there is an- 
 other encapsulated empyema cavity containing 250 cc. of pus. Elsewhere the 
 pleural cavity is obliterated by dense fibrous adhesions. Right pleural cavity. — 
 Contains about 500 cc. of blood-stained fluid. The lung is collapsed and adherent 
 over the posterior surface by fibrinous exudate. Pericardium. — The pericardial 
 sac is obliterated by fresh fibrous adhesions except for two small pockets which 
 contain blood-stained fluid. The heart shows no other abnormahty. Left lung. — 
 The pleura is thick and yellowish with abscess-like spaces in the substance. In 
 places it is lifted up from the lung by accumulations of fluid. Both lobes of the 
 lung are flabby and airless. In the upper lobe there is a small moderately firm 
 but rather spongy area in the posterior part hear the hilum. In general the sub- 
 stance of the lobe is reddish grey in color and in the posterior part there is a 
 grey patch of loose consolidation. There are no small areas of focal consoUdation. 
 The cut surface of the lower lobe is also greyish red, but there are a few hemor- 
 rhagic areas which measure 2 to 4 mm. in diameter and project above the surround- 
 ing lung tissue. The bronchi are very hyperemic, and the bronchial glands are very 
 soft. Right lung. — The pleura is thickened and covered with a thin fibrinous ex- 
 udate which, however, appears as a viscid, bloody fluid between the lung and the 
 diaphragm. The lobes are all easily distended with air. On section the cut surface 
 is greyish red in color and there are no areas of consolidation. Bronchial mucosa 
 is reddened. Bronchial glands are not enlarged. Kidneys. — Right kidney meas- 
 ures 15 by 8 by 4.5 cm. The capsule strips off readily leaving a smooth greyish 
 purple surface on which can be seen numerous small hemorrhages. On section 
 the cortex measures 8 mm. in width, is dark greyish red and opaque, and is studded 
 with numerous small hemorrhages. Glomeruli are visible as small dots. The 
 mucosa of the pelvis is injected. The left kidney is quite similar. 
 
 Cultures from the pleural fluid gave Pneumococcus Type I and Streptococcus 
 hcemolyticus. Those from the left lung gave the streptococcus alone. 
 
 Microscopic Examination. — The left lung shows in the consolidated areas a 
 rather lax filling of the alveoli with leucocytes together with a ragged network of 
 fibrin. There are enormous numbers of organisms, most of which lie free among 
 the leucocytes. They are lanceolate diplococci and seem to possess a definite 
 capsule. There is some infiltration of the bronchial and vessel walls and even of 
 the alveolar walls, but it is chiefly with polymorphonuclear leucocytes, there 
 being relatively few mononuclear cells. There is no marked thickening of the 
 
100 PNEUMONIA IN ARMY CAMPS 
 
 bronchial walls or infiltration of the interlobular septa. There is no organiza- 
 tion of the intraalveolar exudate. Even in distant and relatively unaffected parts 
 of the lung there is some infiltration of the alveolar walls with leucocytes. The 
 pericardium shows a thick layer of fresh granulation tissue binding together the 
 two layers. This is much infiltrated with leucocytes. 
 
 The kidney shows extensive changes in the glomeruli, tubules, and interstices. 
 The glomeruli are large, their capillaries packed with nucleated cells, many of 
 which are leucocytes. In the capsuje of Bowman there are in some cases hyaline 
 masses and strands which stain pink with eosin. In places the capillaries of the 
 glomerular tuft are adherent to the parietal wall of the capsule. The epithelium 
 of the tubules shows rather advanced degenerative changes. The tubules are in 
 many places filled with blood and polymorphonuclear leucocytes. So too the 
 interstitial tissue between the tubules of the cortex is in many places greatly 
 widened and infiltrated with leucocytes. 
 
 Case 40. — B. M. G., age 28 yrs. No history of measles. Caught cold on Jan. 
 29, 1918, and had a chill followed by fever and vomiting. Felt very much nause- 
 ated for several hours. Pain in the right side of chest. Entered the hospital 
 Jan. 30, with dulness and diminished breath sounds in the right chest behind. 
 Left side apparently normal. Sputum bloody with Pneumococci Type IV. 
 Leucocytes 30,000. On Feb. 8 temperature fell to normal, but the next day it rose 
 again, and from that time to death showed great variations. Patient very ill and 
 unconscious. Stiffness of neck and arms. Death Feb. 13, 1918. Autopsy Feb. 
 14, 1918. 
 
 Anatomical Diagnosis: Lobar pneumonia with fibrinous pleuritis. 
 
 Left pleural cavity. — Contains 150 cc. of blood-stained fluid. There are old 
 fibrous adhesions over the whole lung posteriorly and between the lobes. Right 
 pleural cavity. — Entirely obliterated by light fibrinous adhesions which are easily 
 torn through. There is no fluid. Left lung. — Air-containing throughout, but a 
 few bronchi in the posterior portion of the upper lobe contain plugs of exudate. 
 Their walls are thick and greyish. Right lung. — The pleural surface is duU and 
 covered with a thin fibrinous exudate. On section the lung is found to be uni- 
 formly consolidated throughout and grey in color except for a few lobules in the 
 central portion of the lower lobe which are red and loosely consolidated. The 
 alveoli are everywhere filled with plugs of exudate which project above the cut 
 surface giving it a roughened appearance. The interlobular septa are rather con- 
 spicuous in the lower lobe. 
 
 Microscopic Examination. — The left lung shows no alteration except the bron- 
 chial changes in the upper lobe which prove to be tuberculous. Sections through 
 the consolidated right lung show a perfectly uniform filling of the alveoli with 
 masses of exudate composed of leucocytes and fibrin. The fibrin has become 
 compact; the leucocytes are disintegrated. There are also desquamated epithelial 
 cells and some large phagocytes, which contain cell fragments. There are many 
 cocci in short chains which are presumably pneumococci although no cultures 
 
WILLIAM G. MacCALLUM 101 
 
 were made and some of them look like streptococci. The walls of the alveoli are 
 not thickened and the finer structure appears unchanged. The pleura is thick- 
 ened and vascularized and is covered with a thin layer of fibrin. In it there are 
 lymphatics which contain masses of leucocytes and large phagocytes. The inter- 
 lobular septa are wide and dense. 
 
 Bronchi and blood vessels show in many cases a definite mononuclear infil- 
 tration of the walls. Nevertheless in most of the smaller vessels the infiltration is 
 largely in the adventitial lymphatics and is composed of polymorphonuclears. 
 Near the pleura the exudate in many alveoli has undergone organization. 
 
 Case 45. — J. K. S., age 19 yrs. Measles when a child. No eruption lately. 
 Onset Jan. 17, 1918, with a chill, cough, and expectoration of tenacious, blood- 
 streaked sputum. Fever and weakness. Entered the hospital Jan. 18, 1918, 
 with painful dyspnea and dulness over lower lobes of both lungs posteriorly. Leu- 
 cocytes 30,000. Temperature 101-105° F., pulse 100-150, respiration about 
 50-60. Sputum showed Pneumococcus Type III (?). On Jan. 25 he apparently 
 had a fall of temperature by lysis but were still very sick, coughing up purulent 
 material. There was stiU dulness posteriorly over both lungs with diffuse crepi- 
 tant rales. Aspiration negative on both sides. Steadily improved for the next 
 week, but on Feb. 1 there were still some dulness and the same crepitant rales. 
 Sputum now showed Streptococcus hcemolyticus . Feb. 12, lungs fairly clear 
 throughout. There are a few spots of dulness with crepitant rales, but the breath 
 sounds are mostly vesicular. There was a sudden rise in temperature to 106° 
 followed by a fall to 97° on the 14th, when he lapsed into coma and died with 
 symptoms of extreme dyspnea. Death Feb. 18, 1918, 10 a.m. Autopsy Feb. 18, 
 1918, 11 a.m. 
 
 Anatomical Diagnosis: Indurative and organizing pneumonia with abscesses and 
 pleural adhesions. Acute aortic endocarditis. Bilateral abscesses of rectus abdominis. 
 Acute splenic tumor. Duodenal ulcer. 
 
 Right and left pleural cavities. — The cavities contain no fluid. The surfaces are 
 bound together everywhere by organized adhesions which are thin, delicate, and 
 veil-like. Heart. — Pericardium is normal. The heart is not enlarged, contains 
 only postmortem clot. The endocardium is smooth throughout except over the 
 aortic valve. The right coronary and posterior leaflets are occupied by large red- 
 ■ dish yellow masses which in each case bulge in rounded forms both into the sinus 
 and into the ventricle penetrating the leaflet. The right coronary orifice is not 
 involved and the coronary vessels are normal throughout. The other valves are 
 delicate and competent. The heart muscle is greyish red and uniform in appear- 
 ance. Left lung. — The lung is small but very cushiony throughout as though 
 everywhere air-containing. The bronchi exude a thick purulent fluid. On section 
 the tissue is yellowish brown in color and in general air-containing, but through 
 the lower lobe there is a network of greyish yellow strands which are irregidar 
 in outline and firmer than the surrounding tissue. In places these are rather trans- 
 lucent, in other places much more opaque than the adjacent tissue. The upper 
 
102 PNEUMONIA IN ARMY CAMPS 
 
 lobe is more uniformly air-containing, but it too shows a few firm patches like those 
 in the lower lobe. These are not specially related to the bronchi which are practi- 
 cally normal in appearance. Right lung. — This lung is in general air-containing, 
 but there are scattered through the whole organ such strands of condensed tissue 
 as form a network in the left lung. This particular appearance is more distinct 
 after the lung has been hardened when there appear normal spongy portions in the 
 rather small meshes of the close network of denser tissue. This denser tissue has 
 not the appearance of a pneumonic consolidation but suggests the possibility of 
 organization and contraction of an old pneumonic exudate. The upper lobe 
 contains in addition a small group of abscesses each measuring 3 to 5 mm. in 
 diameter and filled with yellow pus. In the anterior part of the lower lobe the 
 tissue is entirely solid, dense, and grey. There are two small abscesses in this 
 area. Stomach and duodenum. — Just below the pylorus there is an ulcer about 1 
 cm. in diameter in the mucosa of the duodenum. The margins are not indurated; 
 the pancreas is not adherent to the base of the ulcer. Rectus abdominis muscle. 
 — There is an abscess measuring 1 by 4 cm. in the substance of each rectus muscle 
 about the junction of middle and lower thirds. These abscesses are exactly sym- 
 metrical in position. They contain a thick, sticky green pus and are lined by a 
 yellowish wall which is stained brown in its deeper portions. 
 
 Cultures at autopsy gave the following results: Right lung, B. influenza, 
 Staphylococcus aureus (hemolytic). Streptococcus hamolyticus , and no pneumo- 
 coccus. Heart valve and abscess in rectus muscle, Pneumococcus Type I. 
 
 Microscopic Examination. — The lungs show practically the same changes. 
 The pleura is slightly thickened and vascular with some infiltration of wandering 
 cells. There are on the surface remains of dense fibrin and groups of the original 
 lining cells of the pleura. 
 
 The interlobular septa are not especially thickened. The bronchi show prac- 
 tically no changes in their walls although most of them are fiUed with leucocytes. 
 The epithelium is in general intact and the connective tissue and muscular layers 
 of the wall are compact and show very few wandering cells. 
 
 On the other hand, the alveolar walls in most places are extraordinarily thick- 
 ened, not by infiltration with mononuclear cells but by a new formation of con- 
 nective tissue. There are, it is true, some mononuclear wandering cells in the 
 substance of these walls and many of them are very large and loaded with yellow 
 pigment. The epithelium is in general complete but much thickened so as to be 
 almost cubical in many places. The alveoli are usually empty but there are 
 places in which they still contain leucocytes and other more extensive places in 
 which they are filled by an organized tissue. This organization of old exudate 
 is not very widespread, however. Such changes in the lung are not uniformly 
 distributed, but alternate with areas in which the alveoli are overdistended with 
 air but are otherwise normal. The exudate both in the bronchi and alveoli con- 
 tains pneumococci, very abundant influenza baciUi, and occasionally a coarse 
 streptothrix. 
 
WILLIAM G. MacCALLUM 103 
 
 Blood vessels and lymphatics are inconspicuous. 
 
 In certain sections of the lung there are found large abscesses with old com- 
 pact masses of fragmented leucocytes forming the center within a dense wall of 
 granulation tissue. 
 
 Case 46. — F. W. S., age 23 yrs. Had measles 10 years ago according to his own 
 account. Had no doctor. Began Feb. S with headache, conjunctivitis, coryza, 
 sore throat, and malaise. On Feb. 6 chills and fever with red papular eruption 
 on chest and face next day. Admitted to hospital Feb. 7. On Feb. 10 had a 
 chill, vomiting, and headache. Temperature 104° F. Feb. 14, signs appeared 
 in lungs for the first time. There was a period of normal temperature between 
 the measles and the pneumonia. Feb. IS, uncomfortable, breathless with a grunt 
 and cyanosis. Dulness over left back and axilla, breath sounds tubular over 
 tip of lower lobe. Bronchophony and whispered pectoriloquy here. Tactile 
 fremitus diminished. Died Feb. 18, 11 a.m. 
 
 Sputum on Feb. IS shows Pneumococcus Type I, also Streptococcus hmmolyticiis . 
 Blood culture on that day gave Pneumococcus Type I. On Feb. 16 cultures of 
 fluid aspirated from the chest gave Pneumococcus Type I and Streptococcus 
 hamolyticus . Thought to have lobar pneumonia with empyema and secondary 
 streptococcus infection. Autopsy Feb. 18, 1 p.m. 
 
 Anatomical Diagnosis: Pneumonia with abscess formation and empyema. Fibrino- 
 purulent pericarditis. 
 
 Left pleural cavity. — Contains an enormous amount of fluid which is olive- 
 green in color, turbid with great flakes of fibrin floating up from the injected 
 pleural surface. Right pletiral cavity. — Contains no fluid; the pleural surfaces are 
 smooth and glistening. Pericardium. — Contains 300 cc. of turbid fluid with float- 
 ing shreds of fibrin. The walls are thickly studded with small hemorrhages and 
 
 covered with a loose fibrinous exudate. Left lung. Completely collapsed and 
 
 flattened against the mediastinal tissues; is flabby and soft, except in the upper 
 part of the lower lobe where there are several firm masses, one of which is 
 necrotic and covered by yellow necrotic pleura. On section it is found that there 
 is an abscess about 12 mm. in diameter in the upper posterior part of the lower 
 lobe. About it is a clearly outlined zone of uniform greyish consolidation. The 
 rest of the lower lobe is collapsed. In the upper lobe the interlobular septa are 
 prominent but there is no consolidation. Bronchi contain purulent fluid but 
 the walls are not thickened nor are the bronchi dilated towards the pleura. 
 Right lung. — Air-containing throughout and normal in appearance. The adrenals 
 are greatly swollen and have lost the distinctness of their zonal marking. 
 
 Microscopic Examination. — The pleura over the left lung is thickened by the for- 
 mation of granulation tissue which is overlaid by a thin but dense layer of fibrin. 
 The interlobular septa are not very conspicuous, although slightly thickened and 
 infiltrated with fibrin and cells. The tissue under the pleura is consolidated, 
 each alveolus being packed with dense fibrin which contains but few cells. These 
 are mostly red corpuscles, desquamated epithelium which is deeply pigmented, 
 
104 PNEUMONIA IN ARMY CAMPS 
 
 and leucocytes. The alveolar walls are greatly thickened by infiltration with 
 various sorts of cells, chiefly mononuclears which act as phagocytes. This dense 
 consolidation extends for a considerable depth. Even where the lung becomes in- 
 sufflated it appears that the air is only 'forced into partly consolidated, partly col- 
 lapsed tissue. The bronchi contain a purulent exudate, but their walls are not 
 much altered from normal, and very slightly infiltrated. 
 
 The lymphatics in the bronchial and vessel walls are distended with leuco- 
 cytes, fibrin, and bacteria. There is a fresh pericarditis with hemorrhages under 
 the pericardial lining cells and a little fibrinopurulent exudate. 
 
 Cultures from pleural fluid, pericardial fluid, both lungs, and blood gave 
 Streptococcus hcemolyticus. No pneumococcus was found in material from these 
 five sources. 
 
 Case 51. — J. L. A., age 35 yrs. Had a cold for several days and was admitted 
 to the hospital Feb. 15, 1918, with chill, fever, and vomiting. Dulness over 
 right lower lobe with crackling rales. No tubular breathing. Faint pleural 
 rub near the right nipple. On Feb. 17 there was a crisis and the temperature 
 sank to normal from 103°. Patient remained in good condition until Feb. 24 
 when he had a chill followed by severe pain in the right side. There were dulness 
 and diminution of breath sound in this region. Sputum contained pneumococcus. 
 On Feb. 27 the tenacious bloody sputum contained Pneumococcus Type II, with 
 influenza bacilli. Mar. 1, patient was very sick, with abdominal distension. 
 Tubular breathing and riles on right side. Blood culture gave Pneumococcus 
 Type II. Sputum gave the same organism. Aspiration of thorax was negative 
 on Mar. 2 and 3. Patient cyanotic; rales over entire chest. Tubular breathing 
 over right lower lobe only. Died Mar. 4, 1918, at 2.15 a.m. Autopsy Mar. 4, 
 1918. 
 
 Anatomical Diagnosis: Lobar pneumonia {right lower lobe) with anemic infarc- 
 tions. Fibrinopurulent pleuritis. Acute peritonitis. Diphtheritic colitis. 
 
 Left pleural cavity. — Contains a few cc. of turbid fluid. The surfaces are fairly 
 smooth except on the posterior portion of both lobes where the lung is collapsed 
 and there are numerous hemorrhages on the surface. Right pleural cavity. — Ob- 
 literated by fresh fibrinous exudate which is especially thick over the upper part 
 of the lung where it contains some fluid. There is no free fluid but it is held in 
 the meshes of the fibrin. The surface of the diaphragm is deeply injected. Peri- 
 cardium. — The pericardium contains about 100 cc. of slightly turbid fluid. There 
 are a few punctate hemorrhages on the heart but the surfaces are smooth and 
 glistening. Peritoneum. — The hepatic flexure of the colon is adherent to the 
 liver, and in this region the peritoneum has lost its gloss and there is a coUec- . 
 tion of purulent fluid. The appendix and pelvic organs are bathed in purulent 
 fluid. There is less fluid on the left side and the peritoneal surfaces are glossy. 
 There is no obvious source for this infection. The mucosa of the intestines is nor- 
 mal throughout except for a few areas of diphtheritic exudate in the region of 
 the ileocecal valve, which stand above the surrounding mucosa and are out- 
 
WILLLA.M G. MacCALLUM 105 
 
 lined by hemorrhage. Left lung. — The lung feels soft throughout although there 
 is some collapse in its posterior part. It was readily insufflated artificially and 
 on section the tissue is normal in appearance thiroughout. There is no thickening 
 of the bronchi. Right lung. — The organ 'is voluminous and heavy. The upper 
 lobe is soft and collapsed and so is the middle lobe except in the anterior part 
 where it is air-containing. The lower lobe is distended with exudate and is solid. 
 The bronchial glands are enlarged and the bronchi contain a purulent exudate. 
 The upper and middle lobes are insufSated readily and normal in structure. The 
 lower lobe on section shows a uniform consolidation in which the alveoli are 
 filled with an exudate of dark reddish grey color. There is no thickening of the 
 bronchial walls and no focal character to the consohdation. There is a firm grey 
 area at the lower margin and the blood vessel passing to this area is thrombosed. 
 There are several patches just beneath the pleura in the more posterior part of the 
 lobe, which correspond sharply with the outlines of lobules and in which the con- 
 solidated tissue is paler and mottled. Over one of these the thick yellow fibrinous 
 exudate is thinned out so that the opacity of the area shows through. All such 
 patches come up to the surface of the lung and are pale grey, sometimes with 
 reddish central portions or small areas of softening. The blood vessels supplying 
 these areas appear to be thrombosed. The interlobular septa are not widened, 
 but there are some beaded distended lymphatics in the lower part of the consoli- 
 dated lobe. These are rendered conspicuous by their opaque yellow contents. 
 
 Cultures at autopsy from the lung showed Pneumococcus Type II atypical with 
 B. infiuenza; peritoneal and pericardial fluids contained Pneumococcus Type II 
 atypical in pure culture. The blood gave Pneumococcus Type II atypical with 
 a Gram-negative colon-like bacillus. 
 
 Microscopic Examination. — The consolidated right lung shows the typical lesions 
 of lobar pneumonia. The pleural exudate is of fibrin not organized. The pleura 
 is not thickened and the original layer of pleural lining cells is still distinguishable. 
 The interlobular septa are wide, infiltrated with fluid and a network of fibrin. 
 There are many polymorphonuclear leucocytes and some mononuclear cells in the 
 meshes of the fibrin. The lymphatics in these septa are enormously distended and 
 plugged completely with clotted masses of leucocytes, blood, and mononuclear 
 cells among which rather numerous pneumococci can be seen. The lymphatics 
 in the pleura and in the adventitia of blood vessels and of bronchi are also dis- 
 tended with the same material, but they are not such huge beaded channels as 
 those related to the septa. 
 
 The bronchi contain leucocytes and fibrin with pneumococci and influenza 
 baciUi, but their walls are not thickened or markedly infiltrated nor is their 
 epithelium destroyed. The alveoli are uniformly filled with a network of fibrin 
 with leucocytes, red corpuscles, and great numbers of pneumococci. Their walls 
 are not thickened or infiltrated, although occasional leucocytes are found there. 
 There are several blood vessels which are completely thrombosed and the areas 
 of lung tissue ordinarily suppHed by them are, with their contained exudate, 
 
106 PNEUMONIA IN ARMY CAMPS 
 
 completely necrotic. These represent anemic infarctions in the consolidated 
 lung. The bronchial glands are enlarged and contain in their sinuses phagocytic 
 cells and pneumococci. 
 
 Case 186. — W. F., age 29 yrs. Began with cough, general malaise, and pain 
 in chest, and was admitted to the hospital on May 2, 1918. Bubbhng rales were 
 found in both lungs. On May 8 there was evidence of meningitis, and 50 cc. of 
 spinal fluid were aspirated, 45 cc. of antimeningococcus serum being injected. 
 On May 11 there were signs of consolidation in the left lower lobe. On May 12 
 patient was irrational and cyanotic. 50 cc. of fluid were aspirated from the 
 left chest. Sputum contained Pneumococcus Type I and influenza bacillus on 
 May 11. Died May 12, 1918. Autopsy 20 hours after death. 
 
 Anatomical Diagnosis: Lobar pneumonia {left lung) with fibrino purulent pleurisy. 
 Acute serofibritious pericarditis. 
 
 Left pleural cavity. — The cavity is practically obliterated by a great mass of 
 greenish yellow fibrin which is thick and shaggy and in the interstices of which 
 there is a large quantity of turbid greenish fluid. This accumulation is chiefly 
 between the lung and the pericardial sac. The lung is bound to the costal 
 pleura by fresh light fibrinous adhesions. There are about 160 cc. of fluid in 
 the space between the lung and the pericardial sac, but the rest of the pleura 
 contains relatively little fluid. The surfaces, where free, are covered with green- 
 ish fibrin in a thin layer. Right pleural cavity. — Contains no fluid. The surfaces 
 are smooth and glistening. Pericardial cavity. — Contains 50 cc. of turbid fluid 
 with shreds of fibrin. The pericardial lining membrane is congested, its surface 
 dull, and covered with a thin exudate of fibrin. Mediastinal tissue. — Infiltrated 
 with yellow purulent exudate. At fhe region of the lower end of the thymus 
 there is an abscess-like accumulation of pus. Left lung. — The lung is large and 
 heavy with its lobes glued together by fibrin which extends over the surfaces as 
 described. The upper lobe is air-containing in its anterior and upper part, 
 but in the region of the hilum and near the cleft between the lobes there are 
 greyish translucent branching areas of consolidation. The bronchi are thick- 
 ened and reddened, but it is not clear that these consolidations are definitely 
 peribronchial. In the lower lobe there are two definite areas of consolidation 
 between which the lung is coUapsed and contains only indefinite nodular foci 
 of consolidation. One of these larger areas occupies the upper posterior por- 
 tion, the other the anterior lower part. They are reddish grey and uniform, 
 showing a granular surface from which a plug of exudate projects from each 
 alveolus. The bronchial glands are large, soft, and edematous, and contain some 
 old yellowish nodules. Right lung. — Everywhere air-containing except for a few 
 small patches of greyish red consolidation in the lower part of the upper lobe. 
 Pharynx and larynx. — Pharynx, epiglottis, and larynx slightly congested. There 
 are no ulcerations in the vocal cords or elsewhere in the larynx. The trachea is 
 slightly reddened. 
 
 Cultures from the heart's blood, left lung, and pericardium gave Pneumococcus 
 Type I. A culture from the left pleura showed Streptococcus hcemolyticus. 
 
WILLIAM G. MacCALLUM 107 
 
 Microscopic Examination. — The left lung shows a thick layer of fibrin on the 
 pleural surface with abundant Gram-positive cocci in short stiff chains scattered 
 throughout. Many of these are in phagocytic cells. The pleura itself overlaid 
 with a dense exudate of fibrin is edematous, slightly thickened, and spread open 
 into meshes and remarkably hyperemic. It appears that there is the begin- 
 ning of organization of the overlying exudate, although the proliferation of connec- 
 tive tissue cells has barely begun. The pleural lining cells are almost all gone; 
 a few can still be seen. The interlobular septa are quite inconspicuous. The 
 lymphatics in the pleura are filled with fibrin and cells with few bacteria. They 
 are not easily found in the substance of the lung. The bronchi are filled with puru- 
 lent exudate; their walls are slightly infiltrated with mononuclear cells. The 
 alveolar walls are nowhere thickened or infiltrated. Their cavities are filled 
 with an exudate of leucocytes, red corpuscles, and fibrin. There are numerous 
 Gram-positive diplococci in places in the alveolar exudate, but almost all of them 
 are enclosed in leucocytes and are apparently partly disintegrated. They, like 
 those seen in the superficial layers of the pleural exudate, look like pneumococci. 
 In addition to these there are in the bronchial exudate great numbers of influenza 
 bacilli. In another section from the left lung there is the same condition of the 
 pleura, but the alveoli are filled not with a fresh exudate of leucocytes but either 
 with fluid or with a dense exudate of fibrin in which are entangled red corpuscles 
 and a few mononuclear cells and leucocytes. These plugs of fibrin are outlined in 
 many cases by a single layer of flat epithelial cells which have grown over them from 
 the alveolar wall. The alveolar walls are thickened by an infiltration with leuco- 
 cytes. In places the epithelium is greatly proliferated and several mitotic figures 
 can be seen in these cells in a single alveolus. They grow until the alveolus is 
 half filled with a mass of epithehum. In this region the walls of the vessels are 
 somewhat infiltrated with mononuclear cells, but those of the bronchi are not much 
 thickened. Enormous numbers of bacteria are found on the surface of the pleural 
 fibrin, but none in the alveolar cavities. 
 
 This is a peculiar condition since certain parts of the consolidated tissue show 
 the alveoli almost but not quite filled with a compact fibrillated mass clothed in a 
 layer of epithelial cells in which the cells are indistinct and in which no bacteria 
 are found, while other areas are filled with exudate containing bacteria. The 
 proliferation of the epithelium recalls the epithelial giant cells described by Hecht 
 in the lungs of children. 
 
 Case 188. — D. W., age 21 yrs. No history of measles. Began gradually about 
 May 3, 1918, with a cough and pain in chest. Drilled for 2 days when pain be- 
 came more severe. Admitted to hospital May 7 when he had a few crepitant 
 rales in the left lower lobe. On May 11 there were tubular breathing, crepitant 
 and moist rales in the right upper lobe, and few rales in the left lower lobe. On 
 May 13 it was evident that there was consolidation of the right upper and middle 
 lobes with many r&les. Diagnosis of lobar pneumonia, left lower, and right 
 upper and middle lobes. Died May 14, 1918, 1.05 a.m. Autopsy May 14, 1918. 
 
108 PNEUMONIA IN ARMY CAMPS 
 
 Anatomical Diagnosis: Lobar pneumonia involving whole right lung (fresh). 
 Organizing lobar pneumonia {left lower lobe). Fibrinous pleuritis. Acute nephritis. 
 
 Left pleural cavity. — There is a fibrinous exudate over the whole lower lobe 
 which binds it to the costal pleura. This extends between the lobes and a 
 short way on the upper lobe ; the remaining pleura over the upper lobe is smooth 
 and without adhesions and contains no excess of fluid. Right pleural cavity. — 
 The whole cavity is obliterated by a fresh fibrinous exudate which glues the sur- 
 faces together. There are a few old adhesions about the apex of the lung. There 
 is no accumulation of fluid. Left lung. — The upper lobe is uniformly air-contain- 
 ing and of normal texture. The lower lobe is nearly solid but there are small 
 spongy patches distributed throughout. These alternate with greyish red 
 irregular areas of solid lung which show a rough surface with projecting alveolar 
 plugs. The bronchi are lined by an opaque ragged layer. In several places but 
 especially near the hilum there are large branching opaque yellow lines which look 
 like obstructed lymphatics. Right lung {Fig. 51). — Large and heavy and con- 
 solidated except in the anterior margin of the middle and lower lobes. It is cov- 
 ered with a thin fibrinous exudate more abundant between the lobes which are 
 glued together. The bronchial glands are very large, pigmented, and flecked with 
 pale grey opacities. The upper lobe on section shows a few small scattered patches 
 of spongy air-containing lung ; these patches amount to only a few alveoli in each 
 case. They are separated by rather mottled greyish red areas of consolidation 
 which are flecked in places with hemorrhages. These areas are practically con- 
 fluent and continuous throughout. The bronchi contain a grey exudate and in 
 places their lining walls are opaque and yellowish red. The middle lobe is more 
 uniformly consolidated, paler than the upper, and with more definite alveolar 
 plugs. It too is flecked with hemorrhages. The lower lobe like the middle is 
 uniformly solid and no spongy areas are seen. It is paler than the upper lobe 
 and does not contain so many hemorrhages. 
 
 Microscopic Examination. — The right lung shows in its consolidated part a 
 pleura covered with dense fibrin. On the outer surface the covering cells are 
 largely destroyed but there is very little evidence of organization. In the 
 interlobar space, however, the lining pleural cells are well preserved in most 
 places. Nevertheless, definite organization of the exudate is going on. The 
 interlobular septa are not conspicuous and lymphatics are scarcely to be found 
 in the sections. The bronchi contain a purulent exudate. Their walls are not 
 thickened or infiltrated. The alveolar walls are not thickened. The alveoli con- 
 tain a rather uniform dense exudate of polymorphonuclear leucocytes, red blood 
 corpuscles, and fibrin. Blood is very abundant in places. In other areas edema 
 predominates. The exudate both in the bronchi and alveoli is loaded with 
 bacteria. The Gram-positive cocci are usually free and are morphologically 
 identical with pneumococci. There are great numbers of minute Gram-negative 
 bacilli, most of which are contained in leucocytes, in the protoplasm of which 
 they are closely packed. These appear to be influenza bacilli. 
 
WILLIAM G. MacCALLUM 109 
 
 The left lung presents a different appearance and it is difficult to decide how 
 this should be interpreted. The consolidation is patchy, with areas which con- 
 tain air. The pleura is thickened by a layer of granulation tissue over which there 
 is fibrin. The interlobular septa are not prominent. The bronchi are filled with 
 a purulent exudate; their walls are slightly spread apart and contain a few wan- 
 dering cells with leucocytes and mononuclear cells. Some of the bronchi show a 
 distinct overdistension of the blood vessels, but the changes are in general slight. 
 The alveolar walls are not thickened or infiltrated with mononuclear cells. The 
 alveoli are not filled with an exudate of polymorphonuclear leucocytes as in the 
 right lung, but contain fluid, red blood corpuscles, desquamated epithelial cells, 
 and dense masses of fibrin containing few cells but overgrown and almost com- 
 pletely covered by epithelium. Such masses are partly replaced by new con- 
 nective tissue. There are some areas in which the alveoli contain leucocytes, 
 but throughout most of the lung the condition is as described. Possibly it repre- 
 sents a much later stage of the lobar pneumonia caused by the pneumococcus 
 than that seen in the right lung, but it is also possible that these changes may 
 depend upon the influenza bacillus. 
 
 The kidney shows a general cloudiness of the cells of the epithelium of consoli- 
 dated tubules, although their free borders are well preserved. There are sev- 
 eral glomeruli in each section in which the capillaries are plugged with hyaline 
 thrombi. In the capsules of all the glomeruli there is a mass of bubble-like 
 coagula and in those which have the thrombosed capillaries there are a few leuco- 
 cytes. The tissue surrounding these glomeruli is infiltrated with red corpuscles 
 and leucocytes. Some of the tubules contain casts and a few polymorphonuclear 
 leucocytes. 
 
 There is little that requires comment in these cases. Most of them 
 were from the Texas epidemic, which is perhaps to be accounted for 
 from the fact that those studies were made in February and March, 
 while the Iowa epidemic was studied in May. 
 
 The cases of lobar pneumonia are described here not because they 
 are extraordinary in any way, but chiefly to show the proportion which 
 they bear to the others and to emphasize the contrast between the 
 anatomical lesions produced by the different organisnjs. 
 
 The distribution of these organisms has already been mentioned. 
 It was Ribbert's idea that in lobar pneumonia one might recognize a 
 lobular arrangement of the exudate with most compact fibrin in the 
 alveoli adjoining the interlobular septa, while the greater number of 
 leucocytes and more especially of pneumococci was to be found in the 
 central portions of the lobule and in the bronchus. This is true to 
 some extent, although the pneumococci are far more uniformly dis- 
 
110 PNEUMONIA IN ARMY CAMPS 
 
 tributed throughout the alveoH and through the whole thickness of 
 the pleural exudate than are streptococci. The latter organisms keep 
 to the bronchial contents and the surfaces of the pleural exudate in 
 interstitial bronchopneumonia and are scattered more like pneumo- 
 cocci in the lobular form. But both pneumococci and streptococci 
 quickly gain the lymphatics and distend them with the resulting exu- 
 date which clots. In lobar pneumonia as in the streptococcal form 
 these lymphatics become very prominent in their course from the 
 pleura as beaded yellow channels. 
 
 In several cases in which there was definite lobar pneumonia and in 
 which blood cultures during life showed the presence of pneumococci 
 (Case 33), or when sputum and pleural fluid contained them (Case 
 36), or sputum, blood, and pleural fluid (Cases 45 and 46), the cul- 
 tures from lungs and other sources at autopsy failed to show them and 
 Streptococcus hamolyticus grew instead. It appears from repeated ex- 
 periences of this kind that the pneumococcus must quickly die out 
 or be overgrown by the streptococcus, or one may find it, as in Cases 
 186 and 188, in the process of being overgrown. 
 
 Curious changes occur in the exudate itself if the first stages of the 
 disease are survived. In Case 25, which was of only 8 days duration, 
 the pneumonia was thought to be in a stage of resolution. This seems 
 questionable, but at any rate few pneumococci could be found in sec- 
 tions, although the fibrin still stained well and they were isolated in 
 culture. But in this lung the infiltration of the alveolar walls with 
 polymorphonuclear leucocytes and the upheaval of the epithehal cells 
 are remarkable. Of a different character are the changes in Case 45 
 in which the pneumonia has left the alveolar walls thickened with 
 fibrous tissue in certain strand-like areas, and the alveoli themselves 
 filled with organized exudate in the form of fibrous bands. The 
 presence of abundant influenza bacilli must be remembered. 
 
 Organization is advanced in one of the lungs of Case 188, and in 
 Case 186 there are alveoli partly filled with dense fibrin from which 
 bacteria have disappeared and nuclei faded. In Case 186 there are 
 in places striking evidences of the proliferation of the epithelium 
 which forms great protoplasmic masses only faintly divided into cells 
 and studded in places with mitotic figures. 
 
WILLIAM G. MacCALLUM 111 
 
 One of the most striking lesions, which may be common enough in 
 any great series, is shown in Case 51 in which the cultures show 
 throughout Pneumococcus Type II. In this uniformly consolidated 
 lung there are many thrombosed blood vessels and as many anemic 
 infarctions which extend to the pleura. They are actual infarctions 
 because the circulation of the lung is embarrassed, and anemic be- 
 cause the lung has become firm like the kidney and there is no longer 
 a chance for blood to ooze into the dead area from adjacent regions. 
 
 No unusual changes were found in the other organs in connection 
 with this form of pneumonia, although there were pericarditis, endo- 
 carditis, peritonitis, and in one case abscesses of the rectus abdominis. 
 
 5. Lobar Pneumonia Combined with Interstitial Bronchopneumonia. 
 
 Case 21. — A. A. McL., age 22 yrs. Entered hospital Jan. 7, 1918, with fever, 
 cough, and sore throat. Conjunctivae injected, no rash, throat clear. Jan. 8, 
 throat very red, marked conjunctivitis, but no rash. Jan. 10 and 11, cough with 
 much expectoration, nausea, and vomiting. Chill and epistaxis. Had acute 
 bronchitis since Jan. 1, otitis media Jan. 25. Jan. 26, there were dulness over the 
 upper right lobe and riles over the entire chest. Very ill until Feb. 4 when he 
 died. Temperature 100-104° F., pulse 100-120, respiration 24-30. Much de- 
 lirium and vomiting. Leucocytes 25,600. Autopsy Feb. S, 1918. 
 
 Anatomical Diagnosis: Bilaierallobar pneumonia ■• Bilateral interstitial hroncho- 
 pneumonia. Fibrinopurulent pleuritis. 
 
 Left pleural cavity. — Free from fluid. Surfaces dulled by thin fibrinous exudate 
 with minute hemorrhages. Right pleural cavity. — Contains a little viscid yellow 
 fluid. Left lung (Fig. 52). — There is an area of consolidation which occupies the 
 posterior part of the upper lobe. The lower lobe is partly collapsed, partly air- 
 containing, the surface greatly injected and flecked with hemorrhages and covered 
 with a fibrinous exudate. On section the upper lobe with the exception of a small 
 part of the mesial surface is uniformly consolidated. The lower lobe shows on 
 section numerous greyish white minute areas of consolidation distributed in 
 groups of two or three, several being found in each lobule. These correspond 
 with the terminal bronchioles. Right lung. — The upper lobe contains a large area 
 of uniform consolidation in which each lobule is sharply outlined and shows each 
 alveolus filled with exudate. Throughout the lower part of the lung there is 
 atelectasis. In this area each interlobular septum is quite distinct and there are 
 numerous minute areas of consolidation in each lobule. These correspond in 
 position with the terminal bronchioles. The same condition is distinctly visible 
 in the lower part of the upper lobe and may be traced into the area of lobar 
 consoKdation. The nodules are numerous throughout the remainder of the lung. 
 
112 PNEUMONIA IN ARMY CAMPS 
 
 Microscopic Examination. — The lungs are practically alike. In the sections 
 which pass through the area of lobar pneumonia the pleura is not thickened. The 
 overlying fibrin is not organized and the pleural lining ceUs are stiU visible. This 
 is true over the portions of the lung occupied by the interstitial bronchopneu- 
 monia, but the pleura is distinctly more vascular and the fibrinous exudate 
 thicker. In the area of lobar consolidation the bronchi contain an exudate of 
 leucocytes; their walls are somewhat infiltrated with mononuclear cells. The ad- 
 jacent and also distant alveoli are uniformly fiUed with the characteristic 
 exudate of pneumococcus pneumonia. The walls are not definitely thick- 
 ened or infiltrated. It is not reaUy possible to recognize areas of interstitial 
 bronchopneumonia embedded in the area of lobar pneumonia, although at the 
 margin where the two conditions join one another it is true they overlap some- 
 what. The alveolar exudate contains many organisms, probably pneumococci, 
 which are in pairs or short stiff chains scattered evenly throughout. Many of 
 these are enclosed in phagocytes. No organization of this exudate has occurred. 
 The interlobular septa are wide and edematous with a loose network of fibrin and 
 many leucocytes and mononuclear cells. There are a few bacteria and often 
 these appear to be streptococci in long flexible chains. The lymphatics injected 
 from the pleura with Berlin blue run in these septa and are often plugged with 
 thrombi rich in leucocytes. There are no great numbers of bacteria to be seen 
 there. The blood vessels have walls somewhat thickened by an infiltration of 
 mononuclear cells. 
 
 As one passes from the area of lobar pneumonia the whole character of the pul- 
 monary alteration changes. The bronchi become conspicuous from the greatly 
 increased thickness of their walls. They are stiU filled with leucocytes and debris 
 of epithehal cells with streptococci, but the walls are very hj^eremic and greatly 
 thickened by the infiltration of mononuclear cells. This extends to the walls of 
 the neighboring alveoli. Such alveoli are filled no longer with a delicate network 
 of fibrin supporting uniformly distributed polymorphonuclear leucocytes, but are 
 found to contain dense plugs of pink-staining fibrin surrounded by mononuclear 
 wandering cells and desquamated epithelium. Streptococci are rarely found 
 there. But organization has occurred everywhere and has advanced so that there 
 are whole patches of the lung in each alveolus of which the exudate is replaced by 
 vascular connective tissue which has retracted and has been covered by alveolar 
 epithelium. The same is true in the bronchi although the connective tissue hes 
 uncovered there in the midst of the exudate. Most of the lung is atelectatic, but 
 the parts intervening between the peribronchial nodules can be blown up with 
 air. 
 
 Pneumococcus Type IV and Streptococcus hcsmolyticus were recovered from the 
 lungs and from the heart's blood. 
 
 Case 23. — F. L. G., age 18 yrs. Taken sick Jan. 15 with cough and pain in 
 left chest and fever. Entered hospital Jan. 19, 1918. DuLness over left lower 
 lobe with tubular breathing and rales. Aspirated Jan. 31, and pus removed 
 from left pleura. Resection of rib Feb. 1. Died Feb. 5. Autopsy Feb .S. 
 
WILLIAM G. MacCALLUM 113 
 
 Anatomical Diagnosis: Interstitial bronchopneumonia with empyema {left lung). 
 Lobar pneumonia {right lung) . 
 
 Left pleural cavity. — Over the 6th left rib in the anterior axillary line is an 
 operation wound 7 cm. long from which projects a rubber tube. A piece of 
 rib has been removed. The pleural cavity is entirely obliterated over the an- 
 terior half by light fibrinous adhesions. The posterior part of the pleura forms 
 a cavity which extends to the vertebral column and contains a small quantity 
 of purulent material. The mediastinal tissues are very edematous. Right pleural 
 cavity. — Contains a small amount of fluid. The surfaces are covered with a 
 thin fibrinous exudate. Left lung. — The lung is collapsed and adherent to the 
 diaphragm where it encloses a pocket of 100 cc. of greenish yellow pus. The 
 surface of the lung is covered with a yellow fibrinous exudate which binds the 
 lobes together. In the posterior portions of both lobes, which are much col- 
 lapsed, there are numerous greyish red foci in the centers of which bronchi are 
 seen filled with purulent exudate. Other reddened areas 2 mm. in diameter seem 
 not to be related to the bronchi. In the upper and posterior part of the lower 
 lobe there is a grey area of consolidation in which each alveolus contains a plug 
 of exudate. Right lung. — The lower lobe is covered with a thin fibrinous exudate 
 while the surface of the upper lobe is smooth. The upper lobe is air-containing 
 throughout, and there are no foci of consolidation. The lower lobe except for 
 the anterior margin is uniformly consolidated. It is grey, firm, and airless and 
 from each alveolus a plug of exudate projects. The lymph glands are moist and 
 swollen. 
 
 Microscopic Examination. — The left lung presents the typical appearance seen 
 in interstitial bronchopneumonia. The pleura is greatly thickened and appears 
 as a layer of granulation tissue with overlying dense fibrin. Much of the lung 
 substance is collapsed. The bronchi are conspicuous because they are fiUed with 
 leucocytes and desquamated columnar epithelium. There are many influenza 
 bacilli among these cells. The walls are greatly thickened and hyperemic and 
 densely infiltrated with lymphocytes, plasma cells, and mononuclear wandering 
 cells of other forms. The adjacent alveolar walls are similarly thickened in the 
 neighborhood of bronchi, vessels, and interlobular septa. Their epithehum is 
 partly desquamated and they contain these cells as well as the mononuclear 
 wandering cells. Where fibrin is found in the alveoli it is not in a dehcate net- 
 work but in dense masses. Organization is well advanced and dense strands of 
 vascularized tissue are found in the bronchi and in the alveoli. In the alveoli 
 hemorrhage is not a prominent contributor to the exudate. There are some 
 red corpuscles but far more of a formless coagulated fluid. The interlobular septa 
 are greatly widened, and where lymphatics are seen they are packed with mono- 
 nuclear cells and leucocytes. 
 
 Sections through the consolidated portions of the lower lobe of the right lung 
 show a thin pleura with an overlying layer of fibrin showing no indication of or- 
 ganization. The bronchi contain an exudate of leucocytes; the epithelium is in- 
 
114 PNEUMONIA IN ARMY CAMPS 
 
 tact or retracted in a ring from the walls. There is no organization of the exudate. 
 The walls of the bronchi are very slightly infiltrated with leucocytes and so too are 
 many of the alveolar walls. It is striking that in this lung the polymorpho- 
 nuclear leucocytes invade the alveolar walls, while in the opposite lung the mono- 
 nuclear cells do so. The alveolar exudate is composed of leucocytes and fibrin. 
 The latter is rather contracted and dense. Many of the alveoli contain fluid. 
 Bacteria which are Gram-positive lanceolate diplococci of considerable elongation 
 are numerous and uniformly scattered throughout the exudate. The influenza 
 baciUi are also present. The interlobular septa are inconspicuous. 
 
 Bacteriological cultures show Streptococcus hcemolyticus in both blood and lung. 
 Nevertheless it seems clear that the bacteria which have caused the lobar pneu- 
 monia in the right lung are pneumococci, both from the anatomical character of 
 the lesion and the morphology of the organisms themselves together with their 
 peculiar distribution. 
 
 Case 31. — J. D. W., age 22 yrs. Began Jan. 14, 1918, with headache, sore 
 throat, coryza, and conjunctivitis. Rash appeared on Jan. 18 when he entered 
 the hospital. Difficulty in breathing developed shortly afterward and tem- 
 perature rose to 102-104° F. Pain in left axilla. Crepitant rales throughout 
 chest. Examination on Feb. 6. Temperature fell to normal on Jan. 29 but rose 
 again suddenly on Feb. 2 and remained above 102° until death. Pulse and 
 respiration changed in parallel way. Dulness over left lung passing into flatness 
 over lower lobe. Tubular breathing with rales over lower lobe. Loud friction 
 rub in left axilla. Right thorax resonant with coarse rales. Cyanosis and slight 
 jaundice. Attempt at aspiration of left pleura resulted in withdrawal of bloody 
 fluid from lung. This contained Pneumococcus Type IV. It was thought that 
 bronchopneumonia followed the attack of measles with acute onset of lobar 
 pneumonia on Feb. 3. Died Feb. 8, 8.30 a.m. Autopsy Feb. 8. 
 
 Anatomical Diagnosis: Clinical history of measles. Interstitial bronchopneumonia. 
 Lobar pneumonia {left) with fibrinopurulent pleuritis. 
 
 Left pleural cavity. — -Contains a considerable quantity of brownish green turbid 
 fluid; the lung is bound by light fibrous adhesions to the diaphragm and pericar- 
 dial sac. Posterior portion of upper lobe and whole lower lobe are covered with a 
 thick fibrinous exudate and so also is the parietal pleura. Right pleural cavity. — 
 There is no excess of fluid and the pleural surfaces are everywhere smooth and 
 ghstening. Left lung {Fig. 53). — The lobes are glued together by yellow fibrinous 
 exudate. The upper lobe is collapsed but not consolidated. The interlobular 
 septa are very distinct. The bronchi are thickened and grey with yellowish white 
 opaque contents. The lower lobe is completely and uniformly consolidated; the 
 cut surface is grey except for a small area in the center of the lobe which is hemor- 
 rhagic. The alveoli are filled with plugs of exudate which stand out above the 
 cut surface giving it a rough granular appearance. The septa are not distinct. 
 The bronchi are filled with a yellow exudate. Right lung. — The upper and middle 
 lobes are cushiony, while the posterior portion of the lower lobe is blue and heavy. 
 
WILLIAM G. MacCALLXJM 115 
 
 There are numerous minute hemorrhages in the pleura about the interlobar clefts. 
 The whole lung is readily insufflated except a small part of the upper lobe. 
 Through all the lobes there are found on section small greyish areas of consoli- 
 dation about 2 to 3 mm. in diameter frequently surrounded by hemorrhage and 
 containing a central bronchiole. One of these patches in the lower lobe is 1 cm. 
 in diameter. 
 
 Microscopic Examination. — The left lung shows a typical lobar pneumonia with 
 uniform densely packed exudate in the alveoli. The bronchi contain a purulent 
 exudate. Their walls are slightly infiltrated with mononuclear cells. The 
 alveolar walls are not thickened; the capillaries appear rather bloodless but con- 
 tain a few megalocaryocytes. The exudate in the alveoli is almost entirely com- 
 posed of leucocytes with very few red corpuscles. The leucocytes are ragged and 
 in certain places reduced to fragments of nuclei. In these places the alveolar 
 walls become indistinct and the capillaries appear to contain hyaline thrombi. 
 There is little to suggest the features of the interstitial bronchopneumonia within 
 the area of lobar consolidation. 
 
 Very few organisms can be found in the alveolar exudate but two or three 
 were found in one alveolus. The right lung shows small bronchi filled with an 
 exudate of leucocytes and with walls much thickened by the infiltration of these 
 cells and mononuclear cells. The walls of the adjacent alveoli are thickened and 
 infiltrated and they contain leucocytes and desquamated epithelial cells and 
 much pigment. The occurrence of pigmented epithelium suggests the possi- 
 biHty of a local obstruction to the outflow of blood or a local chronic passive 
 congestion. There is also a great deal of free blood in these alveoK. The bronchi 
 contain streptococci in pairs and rather long chains. 
 
 Cultures from the blood and right lung showed Streptococcus hcsmolyticus. 
 Those from the left pleural fluid showed Pneumococcus Type IV and the strep- 
 tococcus. 
 
 Case 50. — L. J. W., age 19 yrs. Never had measles. The patient was vacci- 
 nated against typhoid on Jan. 26, 1918, and had a severe reaction. He felt so 
 badly that he was sent to the hospital where after about a week he developed 
 measles, on Jan. 30. Rash lasted 2 days. Then he walked about the ward for a 
 few days when he began to have a pain in his chest and shortness of breath. 
 Coughed and expectorated a great deal and vomited. On Feb. 10 he was found 
 to have a hacking cough but no difficulty in breathing. Did not seem very sick. 
 Dulness over right upper lobe with harsh breath sound. Fine moist rales over 
 both lower lobes behind. On Feb. IS complained of bad stitch in left side; cough 
 short and grunting. Marked dulness in lower left back with suppression of 
 breath sounds. Feb. 16, 1918, 10 cc. of turbid fluid aspirated from left side. 
 Feb. 18, operation for drainage of left side. Died Mar. 2, 1918. Sputum on Feb. 
 14 gave B. influenza and Streptococcus hmmolytictis. Blood culture on Feb. 14 
 negative. Pleural fluid Feb. 16 showed Streptococcus hamolyiicus. Autopsy 
 Mar. 3, 1918. 
 
116 PNEUMONIA IN ARMY CAMPS 
 
 Anatomical Diagnosis: Lobar pneumonia with empyema {left). Interstitial bron- 
 chopneumonia {left) . 
 
 Left pleural cavity. — In the left posterior axillary line there is a wound over 
 the 9th rib from which protrudes a rubber drainage tube discharging a smaU 
 amount of foul smelling fluid. The lung is bound on the anterior margin by 
 light fibrinous adhesions which become more dense as the empyema cavity is 
 approached. Between the anterior margin of the lung and the pericardium there 
 is an encapsulated pocket containing SO cc. of thick greenish yellow pus. The 
 base of the lung is densely adherent to the diaphragm by fibrinous adhesions. 
 The pleura over the anterior part of the lower lobe is covered with a thin fibrinous 
 exudate, while that over the anterior portion of the upper lobe is smooth and 
 glistening. The pleura over the posterior surfaces of the upper and lower lobes 
 is covered by a thick fibrinopurulent exudate, the parietal pleura corresponding 
 with this showing a similar exudate. The empyema cavity contains only a few cc. 
 of pus. Right pleural cavity. — There is no excess of fluid, the lung is free from ad- 
 hesions, and the pleural surfaces are everywhere smooth and glistening. Left 
 lung. — Except for the anterior margin of the upper lobe the whole left lung is 
 consohdated and on section both lobes are greyish red in color with a few 
 scattered areas which are more hemorrhagic. There appears to be no thick- 
 ening of the bronchial walls although the bronchi are filled with purulent mate- 
 rial. The mucosa is hemorrhagic. The bronchial lymph glands are shghtly 
 enlarged. Right lung. — The whole lung is imiformly air-containing except for 
 a slightly firmer patch in the upper lobe which on section is slightly more 
 greyish than the surrounding lung but does not seem definitely consolidated; 
 the alveoh contain no plugs of exudate which project above the surface. There 
 is no thickening of the bronchial waUs although they contain a thick creamy 
 pus. Pericardium. — Contains SO cc. of slightly turbid fluid with a few floating 
 strands of fibrin. The surfaces are slightly injected with an occasional petechial 
 hemorrhage but they have not lost their gloss. 
 
 Cultures from the pericardial fluid gave Streptococcus hcemolyticus in pure cul- 
 ture. Those from the lung, pleural pus, and blood gave also Streptococcus hcemo- 
 lyticus but contaminated with a Gram-negative baciUus. 
 
 Microscopic Examination. — The left lung shows a pleura which is converted 
 into a thick layer of granulation tissue surrounded by dense fibrin. The inter- 
 lobular septa are not conspicuous. The bronchi are scarcely altered. The alveo- 
 lar walls are of normal thickness, the alveoli fiUed with leucocytes. There is little 
 evidence of blood or even of any considerable amount of fibrin. In many places 
 the alveolar walls become scarcely visible and a whole area seems to fuse into a 
 mass of leucocytes. In other places the leucocytes in each alveolus are reduced 
 to a dust of fragments. Many Gram-positive cocci are present among the leu- 
 cocytes in the exudate. These are in very short chains, although there are some- 
 times as many as ten in a chain. They are quite large and elongated and grow 
 rather stiffly and not in sinuous lines. One has the impression that they may be 
 
"WILLIAM G. MacCALLUM 117 
 
 pneumococci and not streptococci, although only the latter were cultivated from 
 the lung and pleura. Their distribution and the nature of the lesion suggest this 
 strongly. There are places in the same lung, however, beneath the thickened 
 pleura but in areas not consoKdated by the alveolar exudate in which the inter- 
 lobular septa are thickened and contain thrombosed lymphatics. The alveoli 
 contain fluid and desquamated epithehum and their walls are infiltrated with 
 mononuclears. The bronchi are greatly thickened and infiltrated with mono- 
 nuclears and show thrombosed lymphatics in their walls. In a word, the whole 
 picture is that of interstitial bronchopneumonia. 
 
 The right lung seems normal. This may be a lobar pneumonia caused by the 
 pneumococcus in which a secondary infection has overgrown the first. 
 
 Case 180. — W. H., age 27 yrs. Negro. Had German measles beginning on 
 Apr. 28, 1918. No history of measles. Entered hospital May 7, when a diag- 
 nosis of lobar pneumonia involving the right lower lobe was made. Sputum was 
 yellow, mucopurulent, and nummular, and was found to contain Pneumococcus 
 Type II atypical, and influenza bacillus. Blood culture on May 8 gave a pure 
 culture of Pneumococcus Type II atypical. There was acute pharyngitis. 
 Died May 11, 1918, 2 a.m. Autopsy May 11, 1918, 10 a.m. 
 
 Anatomical Diagnosis: Clinical history of German measles. Lobar pneumonia 
 {right upper and middle lobes). Interstitial brottchopneumonia {right middle and 
 lower and left lower lobes') . Serofibrinous pleurisy {right) . Ulcerative laryngitis. 
 
 Left pleural cavity. — Contains no fluid. The surfaces are smooth and glisten- 
 ing. There are no adhesions although both costal and pulmonary pleura are ex- 
 tensively scarred. Right pleural cavity. — The surfaces are slightly glued together 
 by a thin fresh fibrinous exudate which contains about 20 cc. of turbid brownish 
 fluid. The surfaces are duUed over the whole lung. Left lung. — The lung is 
 voluminous; the pleural surfaces are smooth. The upper lobe is cushiony and 
 on section is air-containing throughout. In the lower lobe there are some firm 
 patches in the posterior lower margin. Most of the lower lobe is air-containing, 
 but there are some small patches of consoHdation surrounded by zones of col- 
 lapsed lung in the posterior portion. Right lung {Fig. 54) . — ^The lung is very large 
 and heavy, the upper and middle lobes except for the apical and anterior marginal 
 portions being firmly consoHdated. The lower lobe is largely collapsed and feels 
 nodular throughout. On section the whole lower and posterior parts of the 
 upper and middle lobes are consoKdated and greyish red in color, each alveolus 
 containing a plug of greyish exudate. The anterior portions are air-containing in 
 general, but there are small patches of coUaipse and a number of small nodular 
 peribronchial consolidations which can be traced to some extent into the area of 
 lobar consohdation. In the lower lobe the tissue is air-containing and appears 
 normal except in the lower posterior portion where there is a group of firm greyish 
 nodules surrounded by collapsed lung tissue. The bronchi are reddened and 
 contain a turbid frothy fluid. The bronchial glands are enlarged, soft, and grey. 
 The mucosa of the trachea is deeply reddened. Organs of the neck. — ^The base 
 
118 PNEUMONIA IN ARMY CAMPS 
 
 of the tongue and the pharynx in general are reddened. The tonsils are much 
 enlarged. There are ulcerations over the back of the uvula and on the sides of 
 the nasopharynx behind the pillars of the fauces. The posterior aspect of the 
 epiglottis is reddened but not ulcerated, but the vocal cords are rather deeply 
 ulcerated on both sides. The mucosa of the larynx is red and there is a ragged 
 dull opaque area on the right side below the vocal cords. 
 
 Cultures at autopsy showed Streptococcus hmmolyticus in the heart's blood, 
 left lung, and right pleura. Pneumococcus Type II atypical was recovered in 
 culture from both lungs. Gram-positive diplococci were found in smears from 
 the larynx. 
 
 Microscopic Examination. — Section of the vocal cord shows a superficial loss of 
 substance with an inflammatory reaction and numerous streptococci on the sur- 
 face of the necrotic material. There are remnants of coagulated epithelium and 
 many fragmented leucocytes in the surface layer. The ulceration is not very 
 deep, but the streptococci are found in the crevices of the tissue for a considerable 
 distance below the surface. 
 
 Sections from the upper lobe of the right lung show a rather thin but dense 
 fibrinous exudate over the pleura. The surface of this is sprinkled with Gram- 
 positive micrococci in pairs and short chains. 
 
 The interlobular septa are wide and edematous and infiltrated with fibrin. 
 The lymphatics are very large and are filled with blood, leucocytes, and mono- 
 nuclear cells and fibrin. Gram-positive cocci are abundant among these ceUs. 
 
 The bronchi are rather delicate and although their waUs are slightly infil- 
 trated with mononuclear cells they are not thickened. Their lymphatics are 
 plugged in exactly the same way as those of the septa and blood vessel walls. 
 The alveolar walls are normal in thickness. The cavities are filled with a imi- 
 form exudate of polymorphonuclear cells with occasional red corpuscles and a net- 
 work • of fibrin. There are many cocci in pairs evenly distributed and often 
 contained in leucocytes. In the margins of the area of consolidation some of the 
 bronchi are more definitely thickened and infiltrated, and the same condition is 
 found in the walls of some blood vessels. The alveolar exudate remains the 
 same. In the lower lobe the condition is different. The pleural changes are 
 about the same, the interlobular septa wide with lymphatics obstructed by mas- 
 sive thrombi. But the bronchi even to their smallest branches are greatly thick- 
 ened. They contain massed leucocytes with streptococci and numerous influ- 
 enza bacilli. The epithelium is in some instances destroyed and gives place to 
 a necrotic lining layer. The walls -are like a loose vascular granulation tissue 
 with radially placed blood vessels and dense mononuclear infiltration. The alve- 
 olar walls are enormously thickened. New connective tissue has formed in their 
 thickness as in the bronchial walls and they are densely infiltrated. The alveolar 
 cavities are filled with blood in many places especially near the bronchi, but 
 others are filled with fluid. All contain desquamated epithelial cells, some mono- 
 nuclear cells, and dense plugs of fibrin. In many cases there is evidence of or- 
 
WILLIAM G. MacCALLUM 119 
 
 ganization of the exudate, and columns of vascular granulation tissue extend into 
 the bronchioles. 
 
 There is in this case a sharply defined lobar pneumonia in one part of the lung 
 and an equally distinct and characteristic interstitial bronchopneumonia in other 
 parts. From the one the pneumococcus was isolated, from the other the strepto- 
 coccus. The lesions overlap scarcely at all. Influenza bacilli are scattered 
 widely through the lung and are found in the larynx. 
 
 Several cases are separated to form this group because the lung 
 shows a typical lobar pneumonia in one lobe and equally typical 
 lesions of interstitial bronchopneumonia scattered through the re- 
 maining tissue of the same lung. This is especially striking in Cases 
 21 and 180 in which the pneumococcus was cultivated from the area 
 of lobar pneumonia and the streptococcus from the bronchopneumonia 
 lesions. Similarly these organisms could be demonstrated in as far 
 as their morphology permits of their recognition, in characteristic 
 distribution in the corresponding lesions. Influenza baciUi accompany 
 the streptococcus in Case 180 but there are none in Case 21. 
 
 In several cases, Nos. 33, 36, and 45, in which there were definite 
 lesions of lobar pneumonia in the lungs and in which the pneumococcus 
 had been isolated from the blood during life or was isolated from other 
 lesions at autopsy, it had been overgrown and killed by the strepto- 
 coccus in the lungs without the development of t)^ical streptococcal 
 lesions there. In one case, No. 25, in which the pneumococcus was 
 cultivated from the area of lobar pneumonia, it was nevertheless 
 difficult to demonstrate many organisms in the sections. The lung was 
 supposed to be in a state of resolution and it seemed probable that 
 most of the organisms had disappeared. These examples tend to show 
 that the pneumococcus is in many instances at least not a very per- 
 sistent organism and may be supplanted by another such as the strep- 
 tococcus. It is possible, although I think we have no strong evidence 
 to prove it, that in the cases of the present series in which both or- 
 ganisms are present and alive with characteristic lesions produced by 
 each in th? lung, the pneumococcus in producing lobar pneumonia 
 has acted as the forerunner and predisposing agent to infection with 
 the streptococcus. 
 
 The lobar pneumonia in these cases is typical and within its area 
 there are practically none of the interstitial changes which belong 
 
120 PNEUMONIA IN ARMY CAMPS 
 
 to the streptococcus. The pleura over it is thin and shows no granu- 
 lation tissue formation; the bronchi are filled with exudate but other- 
 wise are scarcely altered. One passes abruptly from this into the rest 
 of the lung where typical interstitial bronchopneumonia prevails. 
 Even the pleura seems to become slightly thickened and hyperemic, 
 and the interstitial changes in the bronchi and framework of the lung 
 stand out clearly. But it is difficult to trace these lesions into the 
 area of lobar pneumonia. It is as though the two processes excluded 
 each other, as though the lobar pneumonia once developed formed a 
 barrier to the invasion of the streptococcus but more especially to its 
 power of stirring the tissues to a special type of reaction. One 
 might say that having completed one maneuver of defense the tissues 
 are unable to carry out a different one at once. 
 
 On the whole, one is impressed with the probability that the pneu- 
 mococcus was the first invader. Whether the pneumococcus could 
 gain a foothold in a lung already the seat of extensive lesions caused 
 by the streptococcus seems questionable. 
 
 The following somewhat imperfectly studied case is introduced at 
 this point because it seems important in suggesting the possibihty 
 that the combination of lobar pneumonia and interstitial broncho- 
 pneumonia may be brought about by the pneumococcus alone. In 
 this instance culture from the sputum made 11 days before death 
 showed the predominance of Pneumococcus Type II, and blood cul- 
 ture made on the same day showed the same type of pneumococcus. 
 Unfortunately no cultures were made at autopsy and Streptococcus 
 hamolyticus was never demonstrated. Even in the tissues the organ- 
 isms resemble morphologically the pneumococcus rather than the 
 streptococcus. Influenza bacilli are not present in the sections. 
 Nevertheless there are not only extensive lesions of the type of lobar 
 pneumonia but also characteristic interstitial bronchopneumonic 
 lesions. Since the latter changes have been shown to occur in cases 
 of pure infection with Bacillus influenza, there is no reason to suppose 
 that they could not be produced by the pneumococcus, but if this is 
 accepted as the interpretation of the case, it stands alone in our 
 material. 
 
 Case 196.— R. G., age 25 yrs. Admitted May 5. Died May 18, 1918. On- 
 set about May 1 was gradual with slight pain in the chest, cough, and aching 
 
WILLIAM G. MaCCALLXJM 121 
 
 in back and legs. Physical examination on admission revealed dulness over the 
 right lower lobe, with fine rales, and high pitched expiration. On May 8 there 
 was dulness with distant bronchial breathing over the right upper lobe. May 
 10, delirium. May 11, dulness and bronchial breathing over the left lower lobe. 
 Voice sounds somewhat diminished as though by fluid. Cyanosis. Temperature 
 high in the beginning, 103-10S°F.; later 101-103°. During the last 4 days about 
 104°. Leucocytes 12,000-20,000. Sputum culture on May 7 showed as the 
 predominant organism Pneumococcus Type II. Blood culture on May 7 showed 
 Pneumococcus Type II in considerable numbers. Autopsy May 18, 4 hours 
 after death, by Major Glomset. 
 
 Anatomical Diagnosis: Lobar pneumonia {left upper lobe). Bilateral inter- 
 stitial bronchopneumonia. Acute splenic tumor. 
 
 Left pleural cavity. — There is no accumulation of fluid. The surfaces are glued 
 together by fibrin over the upper lobe of the lung but are easily separated. 
 Right pleural cavity. — No excess of fluid is present. The surfaces of the lower 
 part of the uppejr lobe and the middle lobe are covered with fresh fibrinous exu- 
 date. Pericardial cavity. — Contains 100 cc. of clear straw-colored fluid. The 
 surfaces are smooth. Left lung. — The lung is not collapsed. In the upper lobe 
 there is a patch of coarsely granular consolidation which is greyish in color and 
 involves the upper half of the lobe. The lower lobe is studded with small greyish 
 nodules which are related to the bronchioles and surrounded by dark brown 
 peripheral zones. Right lung. — The upper lobe contains a number of palpable 
 nodules which on section are branched, grey or greyish yellow, and often sur- 
 rounded by hemorrhage. There are in the anterior part two distinct areas of 
 consolidation which are granular with hemorrhagic patches. In the lower 
 lobe there are numerous small nodular areas of opaque yellowish grey. These 
 branch and follow the bronchioles and several are seen within a single lobule 
 (Fig. 55). 
 
 Microscopic Examination. — The area in the left upper lobe shows the alveoli 
 filled with an exudate of leucocytes among which abundant pneumococci are 
 found. In the lower lobe and elsewhere throughout the lung the lesions are 
 typically those described as interstitial bronchopneumonia. 
 
 The pleura is practical^ unaltered. The interlobular septa are widened 
 with some infiltration of cells but especially by the greatly dilated and throm- 
 bosed lymphatics which can be traced into the arterial and bronchial walls. 
 The bronchi are filled with masses of leucocytes among which are Gram-positive 
 diplococci, often separated by a space from the adjacent material and therefore 
 appearing to have a capsule. These are sometimes in short chains of four or 
 six but never in long sinuous chains. Influenza bacilli were carefully searched 
 for, but were not found. The mucosa of the bronchi is greatly swollen and the 
 wall thickened by the formation of a loose, very vascular granulation tissue with 
 abundant mononuclear wandering cells. The adjacent alveoli are filled with 
 dense plugs of fibrin with many red corpuscles and some desquamated epithelial 
 
122 PNEUMONIA IN ARMY CAMPS 
 
 cells. The fibrin is in many places partly or completely organized and clothed 
 in a single layer of epithelium. Hemorrhage of a fresh character is, however, 
 prominent. The alveolar walls and indeed all the tissues of the lung about the 
 infected bronchi are thickened and infiltrated with mononuclear cells. 
 
 In connection with these peribronchial changes there are numerous small 
 patches of consolidated lung tissue in which the alveoli are packed with leuco- 
 cytes together with phagocytic epithelial cells. In these areas the cocci are 
 scattered in great abundance, although elsewhere they are practically con- 
 fined to the bronchial contents and lymphatics. 
 
 6. Old Empyema. 
 
 Case 52. — H. C, age 24 yrs. Entered the hospital Jan. 12, 1918, with fever of 
 sudden onset beginning 3 hours before he was brought to the hospital. Breath- 
 ing was rapid and he was expectorating a reddish foamy sputum. Dulnessover 
 right lower chest behind and breath sounds scarcely audible. On Jan. 15 the 
 breath sounds became tubular over this area, but on Jan. 26 they were again in- 
 audible, although the dulness persisted. Pus was aspirated from the chest and 
 found to contain pneumococci. On Jan. 28 the 8th rib was resected and the 
 thorax drained. The temperature which was irregular and ranged up to 104° F. 
 fell and remained normal until about the middle of February when it again be- 
 came irregularly elevated. On Feb. 22 the 7th rib on the right side was resected. 
 Smears from the pus discharged showed a Gram-positive diplococcus, but no 
 culture was made. After the second operation the patient's temperature became 
 practically normal and he seemed to be doing well. He died suddenly upon 
 sitting up in bed on Mar. 4. Autopsy Mar. 5, 1918. 
 
 Anatomical Diagnosis: Empyema (right) with drainage. Atelectasis of right lung. 
 Embolism of pulmonary artery. 
 
 Left pleural cavity. — Contains no excess of fluid; surfaces are smooth and 
 glistening. Right pleural cavity. — There is a small partly healed wound in the 
 right axillary line over the 8th rib. In the right midscapular line there is a 
 fresher wound from which blood and pus exude through a rubber tube. On 
 opening the thorax it is found that the mediastinal tissues on the right side are 
 infiltrated with a purulent exudate. There are dense adhesions between the base 
 of the lung and the diaphragm and with the costal pleura over the whole 
 lower and anterior part of the lung. From the apex downward and extending 
 half-way forward there is an unobliterated part of the pleural cavity which is 
 lined with thick red velvety granulation tissue and filled with purulent fluid. It 
 is found that the old operation wound extends through the 8th rib, a part 
 of which has been removed. This wound is incompletely healed internally. 
 The second operation wound involves the same rib with removal of another 
 portion. Left lung. — Normal throughout, but in the pulmonary artery there 
 is impacted a folded mass of thrombi which are loose but large enough to 
 
WILLIAM G. MacCALLUM 123 
 
 occlude it. These thrombi are nowhere adherent and the wall of the blood vessel 
 is normal. Right lung. — The pleura on the upper posterior aspect is covered with 
 granulation tissue as described. The bronchi are slightly reddened. On section 
 the lower lobe posteriorly is completely collapsed, but there is no area of con- 
 solidation. The upper and middle lobes are air-containing throughout. The 
 pulmonary artery contains several large thrombus masses one of which is bent 
 upon itself and glued together in that position by a fresh clot. Another is smaller 
 and hollowed out. They are sufficient to occlude the artery, the wall of which 
 is smooth except for one small patch which is slightly roughened. 
 
 The iliac veins are normal on both sides and the walls perfectly smooth. The 
 femoral veins are smooth as far as they could be opened and nothing but liquid 
 blood could be pressed up from them. The pelvic veins show no thrombi. The 
 vena cava is smooth throughout. So too the azygos, the jugulars, subclavians, 
 and other veins seem quite smooth and contain no thrombi. The heart is not 
 enlarged and rather flabby and soft. The endocardium is smooth throughout; 
 the valves are delicate and competent. There are no thrombi. 
 
 Smears from the lung tissue and pleural fluid showed many Gram-positive diplo- 
 cocci often in short chains, but in cultures these were overgrown by a Gram- 
 negative bacillus with putrefactive odor. 
 
 Microscopic Examination. — The right lung shows in part a thick fibrous pleural 
 covering. Where it adjoins the empyema cavity and in the interlobar adhe- 
 sions there is a vascular granulation tissue filled with mononuclear and plasma 
 cells. There are certain round empty spaces surrounded by giant cells, evidently 
 produced by some foreign body. The lung itself is extensively collapsed and the 
 alveoli are fiUed with pigmented epithelial cells. This represents a local chronic 
 passive congestion caused by the collapse. Otherwise no especial alteration of the 
 lung substance is to be observed. The left lung is normal. The thrombi in the 
 pulmonary artery show the characteristic architecture with strands of platelets 
 bordered by leucocytes. They are fresh and show no signs of organization. 
 
 Case 53.— R. J. O'M., age 23 yrs. History negative. On Feb. 1, 1918, he 
 had a severe chill followed by high fever and a pain in his right side and was 
 admitted to the hospital. Physical examination at this time was negative al- 
 though the temperature was 102.4° F. and the pain in the side distressing. On 
 Feb. 6 leucocytes were 23,000 (polymorphonuclears 94 per cent). There was 
 some abdominal pain and rigidity. Temperature ranged from 101-104.6° F., 
 respiration 20-40. On Feb. 12, 150 cc. of pus were aspirated from the left chest 
 and a streptococcus was found in smears and cultures. On Feb. 14 the 7th rib 
 was resected under local anesthesia. Temperature remained as before and patient 
 died on Mar. S, 1918. Autopsy Mar. 6, 1918. 
 
 Anatomical Diagnosis: Multiple pulmonary abscesses. Bilateral empyema. 
 
 Left pleural cavity. — Partly obliterated by fibrinous adhesions in the upper por- 
 tion, while in the lower part the lung is retracted from the chest wall and the 
 pleural surfaces are covered with a thick fibrinopurulent exudate. In the axillary 
 
124 PNEUMONIA IN ARMY CAMPS 
 
 line over the Uth rib there is an incision wound and a portion of the rib has been 
 removed. Very little fluid remains in the cavity. Righi pleural cavity. — Partly 
 obhterated by adhesions, but in the lower portion there are about 300 cc. of 
 purulent fluid. The lower lobe of the lung is collapsed and the pleural surfaces 
 are covered by a yellow fibrinopurulent exudate. The anterior border of the 
 lung is adherent to the pericardium and beneath it is an encapsulated pocket con- 
 taining about SO cc. of turbid fluid. Left lung. — The lower lobe is collapsed, but 
 the whole lung can be inflated artiflcially except the posterior inferior portion of 
 the upper lobe. The upper lobe is air-containing on section except for an area 
 7 cm. in diameter in the posterior part, which is greyish red and consolidated. It 
 includes several soft yellow areas which project above the cut surface. In the 
 lower lobe there are several yellow areas which are irregular in outline and fre- 
 quently confluent and surrounded by consohdated lung. These are fairly firm 
 and contrast sharply with others which measure about 0.5 to 1 cm. and are 
 shghtly elevated. The latter are filled in the center with a dark greyish fluid 
 which can be readily expressed, leaving a crater-hke depression with necrotic sides. 
 They are not surrounded by so much induration as the firmer yellow areas. 
 Bronchial glands are enlarged and softened but contain no foci of caseation. 
 Right lung. — The pleura is slightly thickened and covered with a ribbed fibrinous 
 exudate. In the upper lobe the texture is coarse, and the septa are prominent. 
 There is a yellowish grey flecked consolidation in the lower part of the upper 
 lobe and in the middle lobe. This is not uniform but appears to form a sort of 
 network of alternating spongy and grey translucent tissue often mottled with 
 yellow. There are several abscesses measuring 3 to S mm. or even more and 
 surrounded by a halo of red. The lower lobe is air-containing but has one ab- 
 scess about 1 cm. in diameter in its upper portion. The lymph glands are en- 
 larged and soft. 
 
 Cultures at autopsy gave the hemolytic streptococcus in blood and pleural 
 and pericardial fluid, but in each case it was overgrown by a Gram-positive 
 bacillus. 
 
 Microscopic Examination. — The pleura over the left lung is covered with thick 
 granulation tissue and fibrin. In places the interlobular septa are thickened and 
 contain lymphatics filled with bacteria and leucocytes. In certain areas the 
 lung substance is not much altered except that throughout sharply outlined 
 patches which reach up to the pleura the alveoli are fiUed with a purulent exudate 
 with abundant bacteria. The neighboring alveoli are flattened and collapsed. In 
 the central portion the bacteria form a cloud and the cells including the walls of 
 the alveoli have become necrotic. In other areas there are no abscesses but there 
 is an advanced organization of exudate in the alveoli. The strands of new con- 
 nective tissue are covered with epithelial cells. In the center of some of these 
 strands there are spaces Uned with epithehum which look almost as though it 
 were attempted to produce new alveoli there. 
 
WILLIAM G. MacCALLUM 125 
 
 Case 57.— R. H. H., age 18 yrs. History negative. On Jan. 18, 1918, 
 the patient had a cold followed by weakness and anorexia. Since Jan. 27 
 has felt worse and there has been pain in the right chest. On Feb. 1 had a definite 
 chill and was admitted to the hospital. Physical examination was negative ex- 
 cept for signs of fluid in the right pleural cavity. Temperature 101° F., pulse 98, 
 respiration 23. Leucocytes 23,400. On Feb. 3, 30 cc. of cloudy fluid were aspi- 
 rated from the right chest, and streptococci were found in smears and culture. 
 This was repeated on Feb. 8, and on Feb. 13 the 7th right rib was resected and 
 drainage estabhshed. On Feb. 18 the temperature rose to 102.4° and continued 
 to range between 100° and 104° until death on Mar. 8, 1918. Autopsy Mar. 8, 
 1918, at 1.30 p.m. 
 
 Anatomical Diagnosis: Empyema {right side) with drainage. Atelectasis of right 
 lung. Subacute pericarditis. 
 
 Pericardial cavity. — Contains a small amount of fibrinopurulent exudate. 
 The parietal and visceral layers of the pericardium are granular and covered 
 with fibrin and in a few places are bound together by fraU adhesions. The 
 surfaces are flecked with hemorrhages. Left pleural cavity. — Contains no 
 fluid; the surfaces are smooth and glistening. Right pleural cavity. — In the 
 right axillary line there is a wound 10 by 5 cm. with necrotic edges. This 
 extends into the posterior part of the pleural cavity which contains about 400 
 cc. of dark greenish foul smelling pus. The pleural surfaces are covered with a 
 greenish fibrinopurulent exudate about 5 mm. in thickness. The surfaces are 
 bound together along the anterior margin of the lung. Left lung. — The lung is 
 crepitant throughout and is everywhere easily inflated. On section there is no 
 consolidation and the lung is normal in texture. Right lung. — ^The lung is col- 
 lapsed against the vertebral column and is heavy and airless. There is no con- 
 solidation and the bronchi do not seem to be thickened but lumina are somewhat 
 dilated. The bronchial mucosa is pale grey. Bronchial glands slightly enlarged 
 and soft. 
 
 Cultures are not recorded from this case. 
 
 Microscopic Examination.— The left lung appears to be normal. The right lung 
 is covered with a dense flattened fibrous granulation tissue over which is a thick 
 layer of purulent material. The interlobular septa are very wide and dense like 
 hard old connective tissue. The lymphatics where they are discoverable are em- 
 bedded in this dense tissue, not enlarged but filled with leucocytes and mono- 
 nuclear cells. 
 
 The bronchi are rather thick waUed but have a scarred look as though they had 
 receded from a previous thicker state. They are not densely infiltrated but are 
 commonly full of leucocytes and other cells. The alveolar walls are very thick 
 and are not only infiltrated with mononuclears but show an actual connective tissue 
 thickening. They are usually empty and quite collapsed. 
 
 Case 165. — E. B. deL., age 22 yrs. On Apr. 18, 1918, developed German 
 measles which was succeeded on Apr. 24 by mumps. Present illness began 
 
126 PNEUMONIA IN ARMY CAMPS 
 
 Apr. 27 with a pain in the right chest. Next day the diagnosis of lobar 
 pneumonia with consolidation of the right lower lobe was made and confirmed by 
 radiogram. Empyema developed Apr. 30, and was recognized by aspiration of 
 fluid which contained Streptococcus hcsmolyticus. Died May 4, 1918, at 5.35 a.m. 
 Autopsy May 4, 1918, 5 hours after death. 
 
 Anatomical Diagnosis: Old interstitial bronchopneumonia with empyema {right). 
 Acute fibrinopurulent peritonitis. Phlegmonous laryngitis. 
 
 Left pleural cavity. — Contains very little fluid. The surfaces are smooth anteri- 
 orly but posteriorly are dark blue and covered with hemorrhagic areas and fibrin- 
 ous exudate. Right pleural cavity. — Contains about a liter of turbid fluid which is 
 of the color of pea soup. There are a few floating shreds of fibrin. The right lung 
 is flattened against the outside of the pericardium and is slightly adherent. The 
 surfaces of the pleura are nodular and roughened and covered, except over patches 
 where the lung has adhered, with yellowish exudate. Between the middle and 
 lower lobes there are two pockets fiUed with yellow fibrinopurulent material. 
 Left lung. — The lung is voluminous but the lower lobe is somewhat collapsed. 
 On section the upper lobe is dry, coarse in texture, rather pale red, and every- 
 where air-containing. The anterior and upper parts of the lower lobe are quite 
 similar, but the lower and posterior parts are dark red and collapsed with some 
 projecting nodules which have pale grey centers. The bronchi in this lobe are 
 deeply congested. Bronchial glands moderately enlarged. Right lung.- — Small, 
 pasty, and airless. On section it is almost entirely coUapsed, but there is no 
 consolidation except for a few fairly firm projecting nodules in the lowermost 
 part of the lower lobe. Larynx. — The epiglottis and aryepiglottic folds are greatly 
 swollen and vary in color from greyish red to opaque yellow. On incision the 
 swollen tissues are found to be infiltrated with a purulent fluid. There are shght 
 superficial ulcerations at the brim of the larynx, but the vocal cords are not al- 
 tered. The trachea is slightly reddened. There are opaque yeUow patches on 
 the wall of the pharynx laterally. Tonsils reddened but not swollen. Other 
 organs. — The peritoneum contains a yellow fibrinous exudate which glues together 
 the intestinal loops and is especially abundant over the right lobe of the liver. 
 There are two needle puncture wounds in the right axillary line on a level with 
 the nipple. There are one or two points of hemorrhage in the diaphragm and 
 there is a small opaque yellow point in the Hver surrounded by a hemorrhagic 
 area corresponding fairly well in position with the points of hemorrhage in the 
 diaphragm. 
 
 Microscopic Examination. — The right lung shows a thick layer of granulation 
 tissue replacing the pleura and covered with fibrin. The lung is completely col- 
 lapsed but it can be seen that the bronchi and blood vessel walls are moderately 
 infiltrated with mononuclear cells. The alveolar walls are thickened by a cellu- 
 lar infiltration and their cavities filled in part with fibrin and desquamated epi- 
 thelium. Streptococci are seen in the bronchi associated with large numbers of 
 Gram-positive spore-bearing bacilli. 
 
WILLIAM G. MacCALLUM 127 
 
 Section of the arytenoepiglottic fold of the larynx shows superficial ulcera- 
 tion. There is the most intense phlegmonous inflammation of the underlying 
 tissue, part of which is spread wide by the accumulation of fluid, fibrin, and 
 cells. But all this area of edema is necrotic and is found to contain myriads of 
 streptococci which form a dense feltwork in the tissue. 
 
 No cultures were recorded. 
 
 Case 183. — H. P., age 24 yrs. Began May 2, 1918, with sore throat. Later 
 there was pain in the chest beginning about May 5, and on May 7 the physi- 
 cal signs indicated a lobar consolidation of the right lower lobe. There was 
 dulness to flatness over the right base with bronchophony and bronchial breath- 
 ing. This was confirmed by the radiogram and the suggestion was made that 
 there might be fluid in that pleural cavity. This was made certain by aspira- 
 tion on May 10, and on May 12 a bloody fluid was aspirated from the pericardial 
 cavity. The latter fluid gave on culture a mixture of Streptococcus hcemolytictis 
 and influenza bacillus. The pleural fluid also gave the same combination. Blood 
 culture made on May 7 was negative. Sputum on that day was tenacious and 
 mucoid with no blood and contained both the hemolytic streptococcus and in- 
 fluenza bacillus. Died May 11, 1918, at 4.30 a.m. Autopsy May 11, 12 hours 
 after death. 
 
 Anatomical Diagnosis: Slight pulmonary changes. Bilateral empyema. Acute 
 fibrinopurulent pericarditis. 
 
 Left pleural cavity. — Contains about 150 cc. of yellowish turbid fluid. The 
 surfaces are dull and the lung is slightly adherent to the pericardial sac and to 
 the diaphragm. The tissues of the anterior mediastinum are thickened by 
 an accumulation of turbid fluid. Right pleural cavity. — Contains 1,400 cc. of 
 turbid fluid with much brown sediment which can be stirred up easily. It 
 has the appearance of thin pea soup. The surface of the pleura is deeply 
 reddened and is covered with a layer of yellow fibrin which is easily re- 
 moved. There is a thick layer of fibrin between the lung and the right side of 
 the pericardial sac. Pericardium. — The pericardial sac is enormously thickened 
 and contains about 300 cc. of turbid yellowish fluid. The surface is covered with 
 fibrin which overlies a translucent reddish granulation tissue in which there are 
 some hemorrhages. Left lung. — The lung is heavy and blue, and although the 
 upper lobe is largely air-containing the lower lobe is collapsed and in the posterior 
 portion dark bluish red and pasty. There are patches of hemorrhage under the 
 pleura between the lobes. On section no areas of consolidation are to be found. 
 Right lung.^-The lung feels flabby and is airless. No areas of consolidation can 
 be felt and upon artificial inflation the whole is distended. On section there are no 
 solid portions except for a small encapsulated tubercle at the apex. The bron- 
 chial glands are enlarged and purphsh in color and those at the bifurcation of the 
 trachea contain a few caseous tubercles. The tracheal mucosa is deeply reddened. 
 
 Cultures at autopsy showed the hemolytic streptococcus in the heart's blood, 
 both lungs, right pleura, pericardium, and mediastinum. The influenza bacillus 
 was found in cultures from the right pleura and pericardium. 
 
128 PNEUMONIA IN ARMY CAMPS 
 
 Microscopic Examination. — The pericardial surfaces are covered with an exu- 
 date of fibrin, but there is no underlying granulation tissue. The epicardium is 
 edematous and infiltrated with cells, but the lining pericardial cells are still visible 
 in most places. The superficial layer of the heart muscle is spread apart by an 
 infiltration of leucocytes and mononuclear cells. The mediastinal fat bordering 
 the pleura is edematous and infiltrated with leucocytes. In places the tissue has 
 disappeared and given place to a mass of disintegrated leucocytes. Here strepto- 
 cocci in chains are found in enormous numbers . So too in the cellular debris which 
 adheres to the surface of the fibrin on the pleural side, but no organisms are found 
 in the denser fibrin or in the tissue where it has not undergone necrosis. 
 
 The right lung shows several caseous tubercles in one area and around them 
 the connective tissue structures are dense and thickened. Throughout the rest 
 of the lung, however, there is no definite alteration of interlobular septa, bronchi, 
 or alveoli, except near the surface where there are patches of edema and hemor- 
 rhage with desquamation of the alveolar epithelium and fibrinous exudate in the 
 alveoli; even here the bronchi are little changed. The pleura is converted into 
 a thick layer of granulation tissue with overlying fibrin. 
 
 In the left lung over which the pleura is scarcely thickened it is similarly diffi- 
 cult to find any definite lesion in the lung. There are, however, patches beneath 
 the pleura in which the alveoli are filled with partially organized exudate which is 
 ensheathed in a layer of epithelium. 
 
 This case is one which would offer the greatest support to those who favor the 
 idea of a primary pleurisy. The duration was only 9 days in all and only 6 days 
 after the first pain in the chest was felt. 
 
 The question as to the mode of infection of the pleura has been dis- 
 cussed above and the cases of this group are detailed as examples in 
 which it is difficult to determine the mechanism of infection. There 
 are some who argue for the primary and independent infection of the 
 pleura since they find cases such as these in which it is not easy to 
 observe striking changes in the lungs other than the collapse which 
 is caused by pressure. They must then have recourse to the idea 
 that the bacteria are brought to the pleura by the blood stream be- 
 cause there is scarcely any other way in which the pleura could be 
 infected. Since we have so regularly found cultures of the circu- 
 lating blood sterile, this explanation does not seem acceptable. 
 
 It seems, on the contrary, necessary to hold to the idea that infec- 
 tion takes place by way of the trachea and bronchi and extends thence 
 by way of the lymphatics of the lung (especially after they are ob- 
 structed by thrombi) to the pleura. The difficulty in explaining this 
 origin of the pleurisy in such cases as have just been given is probably 
 
WILLIAM G. MacCALLUM 129 
 
 due to the fact that they are old cases in which the empyema has per- 
 sisted for a long time during which it is conceivable that the pul- 
 monary changes might have been healed. In Case 52 especially, the 
 man was convalescent except for remains of his empyema, but died 
 of pulmonary embolism. In Case 53 abscesses are present but there 
 are remains of an old pneumonia which show as organized exudate, 
 in Case 57 great thickening of the interlobular septa and alveolar 
 walls, in Case 165 even recognizable remains of a diffuse interstitial 
 bronchopnemnonia. Even in Case 183, which was of only 9 days 
 duration and in which the explanation of the pleurisy is especially 
 difi&cult, there are slight changes in the lungs. But in all the others 
 the tracing of the development of the lesions in the lungs which at 
 first are not accompanied by pleurisy, into their later stages in which 
 the IjTuphatics become so strikingly involved and pleurisy arises, 
 seems to show clearly the dependence of the pleurisy upon intra- 
 pulmonary lesions. 
 
 r 
 
 7. Empyema. 
 
 The tabulation and analysis of 53 cases of all the types of pneumonia 
 as they occurred shows an extraordinary frequency of pleurisy with 
 fibrinopurulent effusion which is especially due to the activity of the 
 hemolytic streptococcus. The term empyema which is in common 
 use is not sharply Hmited in its significance, for although it should 
 mean the filling up of the pleural cavity with pus it has been made 
 to do duty in this epidemic for all those forms of pleurisy with exten- 
 sive effusion in which although the exudate becomes distinctly puru- 
 lent if the patient survives long enough, it is frequently in the earlier 
 stages a thin watery brownish turbid fluid with a granular sediment 
 and floating shreds of fibrin. 
 
 The profusion of this fluid exudate is shown crudely by the state- 
 ment that although in thirteen of these cases the chest had been 
 evacuated by resection of a rib and drainage, more than 28 liters of 
 fluid were measured out at the autopsies. 
 
 In only seven of these cases was a fluid exudate in any consider- 
 able quantity found on both sides, and then usually there was a rather 
 small amount only on the less affected side. At the autopsies fluid was 
 found in quantities varying from 10 to 4,000 cc, but it is possible that 
 
130 PNEUMONIA IN ARMY CAMPS 
 
 this does not represent the extremes. 1,000 to 1,500 cc. were com- 
 monly found. 
 
 In the most acute cases in which the streptococcus has produced 
 either peribronchial or lobular lesions in the lungs, the pleura is gener- 
 ally empty and its surfaces are smooth and glistening. This was 
 true in practically all those in which death occurred within 8 days 
 of the onset of the disease and also when fresh lesions developed in 
 the lung opposite to that in which an old affection was found. But 
 when the lung had been infected for 10 days or 2 weeks or more, 
 the pleura nearly always contained an exudate. Then the surface 
 was covered with fibrin overlying petechial hemorrhages, either as a 
 rough thin layer or a thicker shaggy or ribbed coat of yellow or 
 yellowish green. 
 
 The character of the fluid in these earlier cases is so distinctive that 
 at the risk of repetition it should be described once more. Numerous 
 epithets have been apphed to it — it is like thin pea soup, like turbid 
 urine, like unstrained bouillon, like muddy water, but generally like 
 thin pea soup. It has often a greenish cast and the granular sediment 
 which can be stirred up in a cloud tends to settle in the bottom of the 
 pleura. Strands or flakes of fibrin float up in this or hang from the 
 wall. 
 
 Later it rapidly becomes more turbid and thick and assumes a more 
 purulent character, and especially when it is confined in localized 
 areas by adhesions it is often thick whitish green pus. When the 
 pleural cavity has been laid open by resection of the rib the fluid 
 changes somewhat, and if it is secondarily infected with putrefactive 
 organisms it becomes very foul and often blackish green. 
 
 It is most characteristic of the streptococcal pleurisy that organiza- 
 tion of the fibrinous exudate occurs with great rapidity, causing the 
 pleural membrane to become greatly thickened and converted finally 
 into a thick red velvety granulation tissue from which the dense over- 
 lying fibrin can often be brushed off. This is so regular an occur- 
 rence that it is noted in 32 of the 42 cases of streptococcal pneumonia 
 analyzed here, whereas it was observed in only one of the seven cases 
 caused by the pneumococcus and then to a sUght degree only. It is 
 not meant that the organization of exudate and the consequent 
 thickening of the pleural membrane is necessarilv rare in other forms 
 
WILLIAM G. MacCALLUM 131 
 
 of infection, but the rapidity and regularity with which this occurs 
 in the streptococcal infection are striking. The formation of adhe- 
 sions between the lung and the surrounding tissues is of interest to the 
 surgeon. In many cases there were no adhesions when a great quan- 
 tity of fluid exudate had accumulated and then the lung was found 
 collapsed and retracted and flattened against the mediastinal tissues 
 or occasionally, receiving still a little air, floating on the fluid. The 
 extreme coflapse of the lungs and their consequent reduction to a blue 
 pasty mass in which firm nodules were palpable was another striking 
 feature of these cases. 
 
 In many instances there were adhesions which limited the dis- 
 placement of the lung by the fluid or limited the distribution of the 
 fluid. Many of these seemed to be old adhesions which antedated the 
 present disease, others appeared to have been formed in the early 
 days of the disease as a gluing of the surfaces with fibrin, and others 
 still were found in later stages forming a limiting wall about the 
 more or less localized empyema cavity. Occasionally adhesions 
 were obviously due to the presence of an intrapulmonary abscess or 
 other lesion which reached the pleura. In one or two cases such 
 necrotic patches of the pulmonary pleura were well protected by the 
 formation of adhesions. 
 
 The topography of adhesions in connection with well developed 
 empyema is of especial interest. Occasionally what seemed to be old 
 adhesions over the whole upper lobe maintained the position of that 
 lobe, while the lower lobe was forced upward by the fluid collected 
 below. In other cases dense adhesions between parts of the lobe or 
 parts of the pulmonary and costal surfaces left communicating chan- 
 nels connecting with the main cavity. 
 
 Encapsulated pockets of pus are sometimes found and in this series 
 there were thirteen examples of this. In nine cases the pus was im- 
 prisoned between the mesial surface of the lung and the outside of 
 the pericardial sac by adhesions between the anterior margin of the 
 lung and the mediastinum, between the base of the lung and the 
 diaphragm, and between the posterior margin of the lung and the 
 posterior mediastinal tissues. Sometimes as much as 300 cc. of pus 
 were thus enclosed. Of the nine cases three also showed pockets of 
 pus in the adhesions between the lobes of the lung and there were 
 
132 PNEUMONIA IN ARMY CAMPS 
 
 three others in which this occurred alone. In two cases there was 
 found a collection of 100 cc. of green pus between the base of the 
 lung and the diaphragm, and in one or two there were small collections 
 walled off between the lung and chest wall. While many cases 
 showed encapsulation of exudate at autopsy, it is possible that such 
 pockets were broken in some of the thirteen cases in which the pleura 
 had been opened by the surgeon, although in three of the cases in which 
 pockets of pus were found in these situations at autopsy there had 
 been resection of a rib and drainage. On the whole this is not a large 
 proportion, but the failure to discover such pockets is a constant source 
 of anxiety to the surgeon. 
 
 There were eleven cases of lobar pneumonia caused by the pneumo- 
 coccus, among which two were also infected with the streptococcus 
 and showed large purulent pleural exudates. The others had little 
 or no fluid exudate, but the pleural surfaces were glued together by 
 fibrin. There was no organization of the fibrin nor any thickening 
 of the pleural membrane by granulation tissue. 
 
 This stands in sharp contrast to the condition in the streptococcal 
 cases. Indeed in those instances, such as Case 21, in which there 
 were both pneumococcal lobar pneumonia and interstitial broncho- 
 pneumonia in the same lung, the pleura was thickened over the lobe 
 affected by the streptococci but thin over that lobe occupied by the 
 lobar consolidation. 
 
 There was one case, No. 188, of lobar pneumonia with organization 
 of the exudate over which the pleura was shghtly thickened, but 
 another case, No. 45, of long standing in which both pleural cavities 
 were obliterated by fresh fibrous adhesions. In both these cases the 
 lungs contained abundant influenza bacilli. In most of the cases of 
 lobar pneumonia death occurred while the pleura was covered with 
 unchanged fibrin. 
 
 The impression seems to prevail that abscess-like accumulations of 
 pus in the mediastinal tissues are common in the cases of streptococcal 
 empyema. I think, however, that it is usually the pocket of pus 
 between the mesial surface of the lung and the mediastinal tissues 
 which is mistaken for a mediastinal abscess. Nevertheless there was 
 in Case 183 a moderate accumulation of turbid purulent fluid in the 
 tissue of the anterior mediastinum below the level of the remnant of 
 the thymus, and a similar infiltration was observed in Case 52. 
 
WILLIAM G. MacCALLUM 133 
 
 • . 8. Epidemiological Relations. 
 
 The relation of measles to severe and fatal pulmonary inflamma- 
 tions has always been recognized. So too the importance of measles 
 as a predisposing disease in epidemics of pneumonia has been fairly 
 accurately appraised since early times and is definitely mentioned by 
 the writers who describe the pandemic of 1812. 
 
 It is not known, however, in just what way measles facilitates the 
 invasion of the streptococcus. Very httle is known of the actual 
 changes produced by measles in the respiratory tract. In all the 
 great epidemics of measles death appears to have depended largely 
 upon pulmonary infection or else upon the fatal effects of exposure, 
 starvation, and lack of care that accompanied several of the out- 
 breaks among savage people. 
 
 Such autopsies as have been performed upon cases of supposedly un- 
 compHcated measles have left us with only very vague results, and we 
 are in no better position to estimate the part played by measles 
 in the production of the fatal lesions than were those who described 
 the epidemic during the War of 1812, except that we know that in 
 our experience the anatomical changes in the bronchi and lungs are 
 always associated with the presence of Streptococcus hcemolyticus. We 
 know further that this streptococcus can cause the same changes 
 without any predisposing measles and that they are produced in 
 practically identical form in children after whooping cough and diph- 
 theria and, from at least one case in an adult, after scarlet fever. 
 We are therefore incUned to ascribe none of the actual anatomical 
 changes which we can see to measles, but all to the secondary invader. 
 
 Nevertheless it is certain that measles plays an important part. 
 In the Texas autopsy material, if we exclude 7 cases of uncomplicated 
 lobar pneumonia due to the pneumococcus, there were 28 cases of 
 streptococcal pneumonic infection, and of these 15 had recently had 
 measles or were still covered with the rash. At Camp Dodge, Iowa, 
 of 23 cases of streptococcal pneumonia, 8 had just passed through 
 measles and 3 had had German measles. In this epidemic, how- 
 ever, these particular figures are misleading since they depend upon 
 a fresh outbreak of measles pneumonia at the end of a long epidemic 
 in which measles had played no considerable part, the few cases of 
 measles having been thoroughly isolated in a distant barrack. 
 
134 PNEUMONIA IN ARMY CAMPS 
 
 This accidental and sudden flare up of streptococcal bronchopneu- 
 monia in a barrack of measles patients among whom there had pre- 
 viously been no pneumonia, although a great epidemic was prevailing 
 in the general camp, brings out two important points. First, that in 
 this camp the streptococcus had gained a foothold independently of 
 measles and produced an extensive and fatal epidemic of interstitial 
 bronchopneumonia. Second, that when this infection did attack pa- 
 tients ill with measles the bronchopneumonia was much more severe 
 and more quickly fatal. It was among these cases that we found the 
 freshest lesions in patients who had died 4 to 8 days after the begin- 
 ning of the bronchial symptoms. It was almost exclusively among 
 these patients too that we observed the hoarseness and loss of voice 
 which was explained by finding deep ulcerations of the vocal cords 
 and laryngeal walls. 
 
 Therefore' it seems justifiable to conclude that measles brings about 
 a most effective predisposition to infection with the hemolytic strep- 
 tococcus, although the streptococcus can invade and even cause 
 great epidemics without its aid. In addition it may be emphasized 
 that the combination of streptococcus infection with measles seems to 
 produce a far more intense affection than the streptococcus alone, 
 but in this we cannot yet recognize any anatomical changes that are 
 due to measles itself. 
 
 At this point it may be said that these epidemics of streptococcal 
 bronchopneumonia have not been confined to troops in camp but 
 have existed in a more moderate form in the civilian population at 
 many points. Among children the production of typical interstitial 
 bronchopneumonia after measles and whooping cough has been recog- 
 nized at autopsy in a number of cases. 
 
SUMMARY. 
 
 During the winter and spring of 1917-18 tliere has prevailed a great 
 epidemic of measles among the troops quartered in the army camps. 
 It has been especially prevalent in the southern camps. This is 
 probably partly due to the fact that the recruits in the South are 
 largely from remote rural districts and are therefore more susceptible 
 than those in northern camps where the proportion of city dwellers 
 is larger and the intercourse of rural dwellers more extensive. 
 
 Associated with this epidemic in the southern camps there has 
 been a great epidemic of a pecuUar form of pneumonia caused by a 
 hemolytic streptococcus. 
 
 Although this was found to follow measles in a great proportion of 
 cases it also affected men who were recovering from some other 
 disease such as scarlet fever and frequently spread among those who 
 had suffered no predisposing disease. In at least one northern camp 
 in which we worked there had been no significant outbreak of measles, 
 but an independent epidemic of streptococcal pneumonia arose and 
 caused great ravages. Toward its conclusion some patients with 
 measles who were isolated in a distant barrack became infected and 
 died rapidly with a most intense and acute form of the disease. 
 
 Lobar pneimionia caused by the several types of pneumococcus 
 occurred throughout these epidemics, but the number of cases seemed 
 not especially different from what ordinarily occurs during those 
 months of the year. In some cases lobar pneumonia was combined 
 with streptococcal pneumonia. Otherwise there was nothing pecu- 
 liar about the pneumococcal infections. 
 
 The streptococcal infection seems to occur by way of the upper re- 
 spiratory tract and the illness commonly begins with a sore throat, 
 fever, and cough. The physical signs in the lungs are often indefinite 
 until evidence of accumulation of fluid in the chest appears. Dyspnea 
 of the most extreme type especially during inspiration is characteristic 
 and results in a livid cyanosis. Many of the patients become hoarse 
 or lose their voices entirely. They are alert, apprehensive, and sleep- 
 less, and there is often delirium. 
 
 135 > 
 
136 PNEUMONIA IN ARMY CAMPS 
 
 Two main types of pulmonary lesions have been described, al- 
 though these are frequently combined. 
 
 The first, designated interstitial bronchopneumonia, is essentially 
 the result of infection of the bronchioles with large numbers of hemo- 
 lytic streptococci which leads to great changes in their walls and in 
 the adjacent pulmonary tissue. 
 
 The most striking accompaniment of this is a patchy atelectasis or 
 collapse of the lung affecting those portions formerly supphed with 
 air by the obstructed bronchi together with the formation of firm 
 nodules of consohdation about the terminal portions of the bronchi. 
 In addition to this there is extreme engorgement of the blood ves- 
 sels of the lung and hemorrhage into its tissue about the nodules of 
 consolidation. 
 
 The walls of the bronchi themselves become densely infiltrated 
 with mononuclear cells and thickened. Extreme hyperemia and the 
 new formation of blood vessels and of connective tissue add greatly 
 to this thickening and to the deformity of the wall. In some cases 
 the whole lining becomes necrotic and coagulated and constitutes a 
 diphtheritic pseudomembrane. Corresponding with the changes in 
 the bronchial wall are those in the walls of the adjacent alveoli which 
 become greatly infiltrated with mononuclear cells, the alveolar capil- 
 laries are distended with blood, the epithehum is proUferated rapidly 
 and desquamated into the alveolar cavity. These cavities are foimd 
 to be filled in the neighborhood of the bronchus with blood, dense 
 fibrin, a few mononuclear cells, and greater numbers of desquamated 
 epithehal cells. Those which are more distant contain diminishing 
 numbers of these cells but are filled with a thick viscid fluid. This 
 rather gelatinous edema gives a semblance of confluence between 
 these areas of consolidation before it is really completed. But there 
 are many cases in which the changes are restricted to the neighbor- 
 hood of the bronchioles and separated from each other by wide areas 
 of normal air-containing tissue. Streptococci may be found in tan- 
 gled masses in the lumen of each bronchus or bronchiole mingled 
 with the leucocytes of the exudate, but in most instances they are not 
 found in appreciable numbers in the substance of the tissue or in the 
 alveolar contents. 
 
WILLIAM G. MacCALLUM 137 
 
 The lymphatics which run from the pleural network by way of the 
 interlobular septa, bronchial walls, and blood vessel walls to the 
 nodes at the hilum of the lung quickly become a channel for the 
 transport of these bacteria. Great numbers of them are found in 
 these canals and in the sinuses of the lymph nodes at the hilum where 
 they appear to be halted. They cause thrombosis of the lymph chan- 
 nels which become distended to an enormous size and appear to the 
 unaided eye as most conspicuous beaded white strands on the cut 
 surface of the lung extending to connect with the pleural network 
 which may be in places similarly injected and distended with a white 
 infected semipurulent thrombus. These lymphatics are often 2 to 3 
 mm. in diameter, which is not especially greater than the diameter of 
 the normal channels, but they become conspicuous in a way seldom 
 observed because of their yellowish white contents. Sometimes they 
 might almost be confused with the obstructed bronchi. 
 
 It is thought that bacteria extend by growth along these obstructed 
 channels in both directions and thus passing from the lung to the 
 pleura (in a direction opposed to that of the current in unobstructed 
 lymphatics) infect the walls of the pleural cavity and set up the in- 
 tense inflammation with outpouring of fluid exudate. The pleura 
 itself and all the interlobular septa become edematous and permeated 
 by a serofibrinous exudate with wandering cells. 
 
 From the beginning of the infection of the pleura the effusion of 
 fluid exudate becomes a dominant feature of the whole process both 
 in the clinical signs and the anatomical changes. It takes place with 
 extraordinary rapidity and compresses the lung to such a degree as to 
 complete the atelectasis. 
 
 When the exudate is present in such large quantities as 2 or more 
 liters the lung becomes a completely airless pasty blue clump of tissue 
 which is usually plastered against the pericardium or back against 
 the side of the vertebral column. The idea that the opening of the 
 chest with the production of pneumothorax could accentuate the col- 
 lapse of that lung seems rather bizarre, but its ill effects may well 
 come from the influence on the rest of the respiratory tract. 
 
 Later the pleural exudate becomes more distinctly purulent, hav- 
 ing begun as a thin greenish brown turbid^ fluid filled with strepto- 
 cocci and disintegrated leucocytes and shreds of fibrin. 
 
138 PISTEUMONIA IN ARMY CAMPS 
 
 Rapid organization of the inflammatory exudate is everjrwhere char- 
 acteristic. This affects the alveoar and bronchial contents and they 
 are replaced in part by connective tissue. It results particularly in 
 interstitial new growth of connective tissue which thickens the alveolar 
 walls, the bronchial walls, the adventitia of blood vessels, and the 
 interlobular septa. The thrombosed lymphatics become organized 
 and occluded permanently by fibrous tissue so that new ones must 
 eventually be formed, and absorption in the meanwhile is greatly 
 hampered. 
 
 Most striking of all is the rapid organization of the thick layer of 
 fibrin which generally covers the pleura. This results in the forma- 
 tion of thick red vascular granulation tissue on the pleural surface. 
 Adhesions between contiguous surfaces are quickly rendered perma- 
 nent and in the later stages encapsulated pockets of intrapleural origin 
 filled with pus are not infrequently formed and offer difficulties to the 
 surgeon. 
 
 Occasionally large portions of the inflamed lung become necrotic. 
 Such necrotic material is loaded with streptococci and is often dis- 
 charged through the bronchus, leaving a cavity. When this cavity 
 communicates with the pleura too, pneumothorax may result, or if 
 the chest is already open it appears as a bronchopleural fistula. 
 
 Such a disease of the lung betrays at every point its tendency to 
 heal. Everything described above, except perhaps the bronchial exu- 
 date, the pleural exudate, and the intrapulmonary necroses or ab- 
 scesses, partakes of the nature of a barricading process. All the 
 changes tend to limit the advance of the streptococci and indurate 
 the tissue everywhere to this end. The alveolar exudate with its 
 dense fibrin later replaced by connective tissue, the thrombosis of the 
 lymphatics, the thickening and granulation tissue formation in the 
 bronchial walls, interlobular septa, and pleura, and the widespread 
 hyperplasia of lymphoid tissue throughout the lung are all evidences 
 of a considerable power of resistance which allows the body time for 
 defence. The infection is fairly well locahzed in the respiratory 
 tract and there is no septicemia until perhaps the last few hours of 
 life. Other organs therefore suffer Httle. The upper respiratory 
 tract is all infected, and ulcerative changes have been described. 
 
WILLIAM G. MacCALLXJM 139 
 
 The second type, designated arbitrarily lobular pneumonia, is com- 
 posed of cases in which the streptococci invade in the same way. One 
 does not know how to distinguish the symptoms and yet at autopsy 
 although sometimes even the lungs may look much the same at a 
 casual glance they are really different. There are no firm peri- 
 bronchial nodules. Instead there are patches of consolidation in 
 which the alveoli are filled with blood and leucocytes and enormous 
 quantities of streptococci. No interstitial changes are there and no 
 signs of resistance; widespread necrosis occurs with final destruction 
 of areas of lung substance. Hemorrhage about these areas is usual 
 and there is often pleural effusion but without any organization of the 
 exudate. There are many cases in which this lobular pneumonia 
 occurs in the pure form, but there are many others in which it is 
 found side by side with the interstitial bronchopneumonia. , They are 
 different expressions of reaction to the same infection, but in these the 
 reaction is very feeble. There is nothing new in the forms of pneu- 
 monia in this epidemic. They have evidently existed always and 
 with a fair degree of probability one may trace them back to the 16th 
 century. More recognizable descriptions date from 1812, and per- 
 fectly clear ones from Delafield in 1884. 
 
 Addendum. 
 Significance of the Presence of Influenza Bacilli. 
 
 Since this paper was sent to press another and much greater epi- 
 demic has occurred with appalling mortality from pneumonia. The 
 original disease in this epidemic has been spoken of as influenza, 
 and measles has played no part. Attention has been concentrated 
 upon the influenza bacillus of Pfeiffer since it is commonly regarded 
 as the cause of influenza, and much new information has already been 
 published as to the biology of that organism. 
 
 Whatever its true status in connection with the epidemic disease, 
 influenza, we have at least learned from numerous autopsies that it 
 must be regarded as a serious pathogenic agent in the production of 
 pneumonia and that it may be found in pure culture associated with 
 a form of pneumonia which is practically identical with the inter- 
 
140 
 
 PNEUMONIA IN ARMY CAMPS 
 
 stitial bronchopneumonia described above, except in the absence of 
 empyema. It is, however, often found with pneumococci and strep- 
 tococci in other types of pneumonia. 
 
 The invention of a new stain for Gram-negative bacteria by Dr. 
 Goodpasture and its successful combination with Weigert's stain 
 for Gram-positive organisms have made it possible to restudy the 
 tissues from the epidemic described above with the assurance of being 
 able to demonstrate influenza bacilli in the tissues whenever they 
 were present and to distinguish them easily from streptococci, pneu- 
 mococci, and other Gram-positive bacteria. This rests, of course, 
 entirely upon the basis of their morphology, but in many cases it is 
 supported by the results of cultures from sputum or even from the 
 lungs. 
 
 I have, therefore, taken the opportunity afforded in the correction 
 of the proof to introduce notes on the presence of these organisms, 
 although the general discussion is left unchanged. 
 
 It is evident that owing to unsatisfactory culture methods influ- 
 enza bacilli were missed in many cases, and it is now proved that the 
 bacilli can be demonstrated in the bronchioles and occasionally in 
 the alveoli of the Ixmgs in 16 of 48 acute cases, while in at least 6 
 other cases they were present in the sputum. Their distribution 
 among the groups of cases is interesting. 
 
 Type of pneu^nouia. 
 
 Total No. 
 of cases. 
 
 InQuenza 
 
 bacilli 
 present in. 
 
 Case Nos. 
 
 
 16 
 9 
 7 
 
 11 
 
 S 
 
 5 
 4 
 
 5 
 
 2 
 
 15, 32, 37, 49, 191 
 
 
 29, 35, 181, 205 
 
 
 
 
 33, 45, 51, 186, 188 
 
 Interstitial bronchopneumonia and lobar pneu- 
 monia 
 
 23, 180 
 
 It may be said that they tend to be associated with the interstitial 
 and organizing processes, since even some of the cases of lobar pneu- 
 monia (Nos. 45, 186, and 188) show a tendency to organization of the 
 exudate and thickening of the interstitial tissue. One might leap to 
 the conclusion that they are responsible for this process or even that 
 they are the forerunners of the streptococcus and pneumococcus in- 
 
WILLIAM G. MacCALLUM 141 
 
 fections. It is even suggested in the face of the obvious influence 
 of the epidemic of measles that during the whole period of the win- 
 ter epidemic there may have been influenza which predisposed to 
 secondary streptococcus infections. But there remain the facts that 
 most of the cases show no influenza bacilli and that in those which 
 are most typical of the form of interstitial bronchopneumonia (Nos. 
 34, 41, 184, etc.) the most painstaking search through many sections 
 has failed to reveal any of these organisms. It is true that Case 
 37 shows relatively few streptococci and great numbers of influenza 
 bacilli and is probably to be regarded as essentially produced by the 
 influenza bacillus. But in all the others the streptococcus is the 
 predominant organism, if we except Case 196 in which there were no 
 influenza bacilli and in which the lesion seems to have been caused 
 by pneumococci. 
 
 I think it must be recognized that the interstitial forms of bron- 
 chopneimionia can be produced by various organisms, including 
 pneumococci, streptococci, and the influenza bacillus. Where there 
 is a mixed infection it is difficult to assign to each its exact part in 
 the process, but it appears that in spite of the frequent presence of 
 the influenza bacillus this was essentially an epidemic of streptococcal 
 pneumonia. 
 
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142 PNEUMO^rIA in army camps 
 
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WILLIAM G. MacCALLUM 143 
 
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 EXPLANATION OF PLATES. 
 Plate 1. 
 
 Fig. 1. Case 14. Interstitial bronchopneumonia. Early bronchial lesion with 
 surrounding hemorrhage. 
 
 Plate 2. 
 
 Fig. 2. Case 14. Interstitial bronchopneumonia. Early bronchial lesion. 
 Beginning organization of exudate in bronchial lumen. 
 
 Plate 3. 
 
 Fig. 3. Case 15. Interstitial bronchopneumonia. Infiltration of alveolar 
 walls and perivascular tissue. 
 
 y Plate 4. 
 
 Fig. 4. Case 16. Interstitial bronchopneumonia. Right lung with inter- 
 lobar empyema pocket. 
 
 Plate 5. 
 
 Fig. 5. Case 16. Interstitial bronchopneumonia. Atelectasis with organi- 
 zation of bronchial exudate. 
 
 Plate 6. 
 
 Fig. 6. Case 32. Interstitial bronchopneumonia. Early bronchial and peri- 
 bronchial lesion. 
 
 Plate 7. 
 
 Fig. 7. Case 32. Interstitial bronchopneumonia. Bronchial and peribron- 
 chial infiltration. 
 
 Plate 8. 
 
 Fig. 8. Case 34. Interstitial bronchopneumonia. Portion of left lung show- 
 ing prominent interlobular septa and peribronchial nodules. 
 
 Plate 9. 
 
 Fig. 9. Case 34. Interstitial bronchopneumonia. Portion of left lung show- 
 ing prominent interlobular septa and many distended lymph channels which 
 appear as white beaded canals. 
 
144 PNEUMONIA IN ARMY CAMPS 
 
 Plate 10. 
 
 Fig. 10. Case 34. Interstitial bronchopneumonia. Interlobular septum with 
 great distension of lymph channels by an infected thrombus. 
 
 Plate 11. 
 
 Fig. 11. Case 34. Interstitial bronchopneumonia. Thickening and infiltra- 
 tion of the wall of a small bronchus. 
 
 Plate 12. 
 
 Fig. 12. Case 34. Interstitial bronchopneumonia, showing dislodgement of 
 the epithehum of the bronchus, the great thickening and infiltration of the wall, 
 and changes in the adjacent alveoK. 
 
 Plate 13. 
 
 Fig. 13. Case 37. Interstitial bronchopneimionia. Right lung, showing the 
 nodular character of the peribronchial lesions. The spleen is included. 
 
 Plate 14. 
 
 Fig. 14. Case 37. Interstitial bronchopneumonia. Infiltration of bronchial 
 wall which has lost its epithelium. Dense fibrinous plugs in the adjacent alveoli. 
 
 Plate 15. ■ 
 
 Fig. 15. Case 39. Interstitial bronchopneumonia. Right lung. 
 
 Plate 16. 
 Fig. 16. Case 41. Interstitial bronchopneumonia. Left lung. 
 
 Plate 17. 
 
 Fig. 17. Case 41. Interstitial bronchopneumonia. Right upper lobe show- 
 ing large nodules of consolidation about the bronchi. 
 
 Plate 18. 
 
 Fig. 18. Case 41. Interstitial bronchopneumonia. Bronchial thickening 
 produced by lymphoid hyperplasia and great infiltration of the wall. 
 
 Plate 19. 
 
 Fig. 19. Case 41. Interstitial bronchopneumonia. Infiltration of bronchial 
 wall. ConsoUdation of adjacent tissue. 
 
 Plate 20. 
 
 Fig. 20. Case 41. Interstitial bronchopneumonia. Small bronchus with 
 thickened and hyperemic wall. Surrounding consolidation. 
 
WILLIAM G. MacCALLUM 145 
 
 Plate 21. 
 
 Fig. 21. Case 178. Interstitial bronchopneumonia. Early stage with peri- 
 bronchial hemorrhages. 
 
 Plate 22. 
 
 Fig. 22. Case 178. Interstitial bronchopneumonia following measles. Ul- 
 ceration of vocal cords. 
 
 Plate 23. 
 
 Fig. 23. Case 178. Section passing through pleura and interlobular septum 
 with lymphatic canal, showing valves directed away from the pleura. 
 
 Plate 24. 
 
 Fig. 24. Case 178. Interstitial bronchopneumonia. Bronchus with thick- 
 ened wall, showing masses of streptococci in the purulent contents of the lumen. 
 Infiltration of adjacent alveolar walls. 
 
 Plate 25. 
 
 Fig. 25. Case 184. Interstitial bronchopneumonia. Left lung. 
 
 Plate 26. 
 
 Fig. 26. Case 184. Interstitial bronchopneumonia following measles. Ul- 
 cerative laryngitis. Ulcers of vocal cords and epiglottis. 
 
 Plate 27. 
 
 Fig. 27. Case 184. Interstitial bronchopneumonia. Necrosis of mucosa of 
 bronchus. Infiltration and edema of bronchial wall. Infiltration and collapse of 
 adjacent alveoli. 
 
 Plate 28. 
 
 Fig. 28. Case 184. Interstitial bronchopneumonia. A mitotic figure is shown 
 in an epithehal cell of the alveolar lining. 
 
 Fig. 29. Case 184. Interstitial and lobular pneumonia. Bronchial wall 
 with hyperemia and infiltration and necrosis of the mucosa. Nearby is a patch 
 of lobular pneumonia. 
 
 Plate 29. 
 
 Fig. 30. Case 191. Interstitial bronchopneumonia. Left lung. 
 
 Plate 30. 
 
 Fig. 31. Case 29. Interstitial bronchopneumonia. Thickening, infiltration, 
 and hyperemia of bronchial wall . 
 
 Plate 31. 
 
 Fig. 32. Case 29. Interstitial bronchopneumonia. Infiltration of bronchial 
 wall and adjacent tissue. 
 
146 PNEUMONIA IN ARMY CAMPS 
 
 Plate 32. 
 
 Fig. 33. Case 29. Interstitial bronchopneumonia. Induration of interlobu- 
 lar septum and of alveolar walls. Thrombosed lymphatic in the septum. 
 
 Plate 33. 
 
 Fig. 34. Case 29. Interstitial bronchopneumonia. Infiltration of bronchial 
 wall. Consolidation of adjacent tissue. 
 
 • Plate 34. 
 
 Fig. 35. Case 181. Interstitial bronchopneumonia. Right lung with cavity 
 in the upper lobe and bronchiectases in the lower. 
 
 Plate 35. 
 
 Fig. 36. Case 194. Interstitial bronchopneumonia, combined with lobular 
 pneumonia. Hemorrhagic lobular area in lower lobe, 
 
 ' • Plate 36. . 
 
 Fig. 37. Case 205. Bilateral hyaline degeneration of rectus abdominis muscle 
 with rupture and hemorrhage. 
 
 Plate 37. 
 
 Fig. 38. Case 205. Interstitial bronchopneumonia. Left lower lobe with 
 projecting peribronchial nodules. 
 
 Plate 38. 
 
 Fig. 39. Case 205. Combined interstitial bronchopneumonia and lobular 
 pneumonia. 
 
 Plate 39. 
 
 Fig. 40. Case 20. Lobular pneumonia with large area of necrosis and hemor- 
 rhage. Distended lymphatics run to the pleural surface. 
 
 Plate 40. 
 
 Fig. 41. Case 26. Lobular pneumonia with empyema. Distended lym- 
 phatics run to the pleural surface. Left lung. 
 
 Plate 41. 
 
 Fig. 42. Case 55. Lobular streptococcal pneumonia with extensive necroses 
 and empyema. Left lung. 
 
 Plate 42. 
 
 Fig. 43. Case 55. Lobular streptococcal pneumonia with abscesses. Right 
 lung. 
 
WILLIAM G. MacCALLUM 147 
 
 Plate 43. 
 
 Fig. 44. Case 187. Lobular streptococcal pneumonia. The consolidation is 
 confluent in the upper lobe but focal in the lower part of the lung. Left lung. 
 
 Plate 44. 
 
 Fig. 45. Case 187. Confluent lobular streptococcal pneumonia. Hyaline 
 thrombi in alveolar capillaries. 
 
 Fig. 46. Case 187. Lobular streptococcal pneumonia. One alveolus from 
 the preparation shown in Fig. 45. The hyahne fibrinous thrombi in the capil- 
 laries stain deeply and streptococci are seen with leucocytes in the alveolus. 
 
 Plate 45. 
 Fig. 47. Case 192. Hemorrhagic lobular pneumonia. Left lung. 
 
 Plate 46. 
 Fig. 48. Case 192. Hemorrhagic lobular pneumonia. Right lung. 
 
 Plate 47. 
 Fig. 49. Case 192. Hyaline degeneration in the rectus abdominis muscle. 
 
 Plate 48. 
 
 Fig. 50. Case 25. Lobar pneumonia. Pneumococcus infection. Infiltra- 
 tion of alveolar walls with leucocytes. 
 
 Plate 49. 
 
 Fig. 51. Case 188. Lobar pneumonia. Pneumococcus Type H and 5. 
 influenza. Right lung. 
 
 Plate 50. 
 
 Fig. 52. Case 21. Combination of lobar pneumonia (pneumococcus infec- 
 tion) with interstitial bronchopneumonia (streptococcus infection). Left lung. 
 
 Plate 51. 
 
 Fig. 53. Case 31. Typical lobar pneumonia. Pneumococcus Type IV. Left 
 lung. The other lung showed interstitial bronchopneumonia with streptococcus 
 infection. 
 
 Plate 52. 
 
 Fig. 54. Case 180. Combined lobar pneumonia and interstitial broncho- 
 pneumonia in the same lung. Pneumococcus Type II and streptococcus. 
 Right lung. 
 
 Plate 53. 
 
 Fig. 55. Case 196. Interstitial bronchopneumonia. Lobar pneumonia in the 
 opposite lung. Pneumococcus Type II. 
 
MONOGRAPH NO. 10. 
 
 PLATE 1. 
 
 Fig. 1. 
 
 (MacCallum: Pneumonia in army camps.) 
 
MONOGRAPH NO. 10. 
 
 PLATE 2. 
 
 Fig. 2. 
 
 (MacOllltim: Pm-'umoni;! in army camps.) 
 
MONOGRAPH NO. 10. 
 
 PLATE 3. 
 
 (MacCallum: Pneumonia in army camps.) 
 
MONOGRAPH NO. 10. 
 
 PLATE 4. 
 
 Fig. 4. 
 
 (MacCallum: Pneumonia in army camps.) 
 
MONOGRAPH NO. 10, 
 
 PLATE 5. 
 
 
 (MacCallum: PiieumonJa in army camps.) 
 
MONOGRAPH NO. 10. 
 
 PLATE ( 
 
 Fig. 6. 
 
 (MacCallum: Pneumonia in army camps.) 
 
MONOGRAPH NO. 10. 
 
 PLATE 7. 
 
 Fig. 7. 
 
 (MacCallum: Pneumonia in army camps.) 
 
MONOGRAPH NO. 10. 
 
 PLATE 8. 
 
 Fig. 8. 
 
 (MacCallum: Pneumonia in army camps.) 
 
MONOGRAPH NO. 10. 
 
 PLATE 9. 
 
 Fig. 9. 
 
 (MacCallum: Pneumonia in army camps.) 
 
MONOGRAPH NO. 10. 
 
 PLATE 10. 
 
 Fig. 10. 
 
 (MacCaUum: Pneumonia in army camps.) 
 
MONOGRAPH NO. 10. 
 
 PLATE 11. 
 
 Fig. U. 
 
 (MacCallum: Pneumonia in 
 
 army camps,) 
 
MONOGRAPH NO. 10. 
 
 PLATE 12. 
 
 •/ -.A 
 
 :• ' ' '. ■^- '■ 
 
 , . tiV ■■'■■■'■ 
 
 (MacCallum: Pneumonia in army camps.) 
 
MONOGRAPH NO. 10. 
 
 PLATE 13. 
 
 Fig. 13. 
 
 (MacCallum: Pneumonia in army camps.) 
 
Monograph no. io 
 
 PLATE 14. 
 
 Fig. 14. 
 
 (MacCallum: Pneumonia in army camps.) 
 
MONOGRAPH NO. 10. 
 
 PLATE 15. 
 
 Fig. 15. 
 
 (MacCallum: Pneumonia in army camps.) 
 
Fig. 16. 
 
 ('Mnrra.lliim: Pnenmonia in aimv crmns.'t 
 
MONOGRAPH NO. 10 
 
 PLATE 17. 
 
 Fig. 17. 
 
 (MacCallum: Pneumonia in army camps.) 
 
MONOGRAPH NO. 10. 
 
 PLATE 18. 
 
 (MacCallum; Pneumonia in army camps.) 
 
MONOGRAPH NO. 10. 
 
 PLATE 19 
 
 Fig. 19. 
 
 (MacCallum: Pneumonia in n.rmy camps.) 
 
MONOGRAPH NO. 10. 
 
 PLATE 20. 
 
 Fig. 20. 
 
 (MacCallum; Pneumonia in army camps.) 
 
MONOGRAPH NO. 10. 
 
 PLATE 21. 
 
 Fig. 21. 
 
 (MacCallum: Pneumonia in army camps.) 
 
MONOGRAPH NO. 10. 
 
 PLATE 22. 
 
 Fig. 22. 
 
 (MacCallum : Pneumonia in army camp3.) 
 
MONOGRAPH NO. 10. 
 
 PLATE 23. 
 
 Fig. 23. 
 
 (MacCallum: Pneumonia in army camps.) 
 
MONOGRAPH NO. 10. 
 
 PLATE 24. 
 
 Fig 24. 
 
 (MacCallum: Pneumonia in army camps.) 
 
Fig. 25. 
 
 (MacCalKim: Pneumonia in army camps ) 
 
MONOGRAPH NO. 10. 
 
 PLATE 26. 
 
 Fig. 26. 
 
 (MacCallum: Pneumonia in army camps.) 
 

MONOGRAPH NO. 10. 
 
 PLATE 27. 
 
 Fig. 27. 
 
 (MacCallum: Pneumonia in army camps.) 
 
Fig. 28. 
 
 Fig. 29. 
 
 (MacCallum: Pneumonia in army camps.) 
 
MONOGRAPH NO. 10. 
 
 PLATE 29. 
 
 Fig. 30. 
 
 (MacCallum: Pneumonia in army camps.) 
 
MONOGRAPH NO. 10. 
 
 PLATE 30. 
 
 Fig. 31. 
 
 (MacCallum: Pneumonia in army camps.) 
 
MONOGRAPH NO. 10. 
 
 PLATE 31. 
 
 Fig. 32. 
 
 (MacCallum: Pneumonia in army camps.) 
 
MONOGRAPH NO. 10. 
 
 PLATE 32. 
 
 (MacCallum; Pneumonia in army camps.) 
 
PLATE 33. 
 
 MONOGRAPH NO. 10. 
 
 Fig. 34. 
 
 (MacCallum: Pneumonia in army camps 
 
MONOGRAPH NO. 10. 
 
 PLATE 34. 
 
 (MacCallum: Pneumonia in army camps.) 
 
MONOGRAPH NO. 10. 
 
 PLATE 35. 
 
 Fig. 36. 
 
 (MacCallum: Pneumonia in army camps.) 
 
MONOGRAPH NO. 10. 
 
 PLATE 36. 
 
 Fig. 37. 
 
 (MacCallum: Pneumonia m army camps.) 
 
MONOGRAPH NO. 10. 
 
 PLATE 37. 
 
 Fig. 38. 
 
 (MacCallum; Pneumonia in army camps.) 
 
MONOGRAPH NO. 10. 
 
 PLATE 38 
 
 Fig. 39. 
 
 (MacCallum: Pneumonia in army camps.) 
 
MONOGRAPH NO. 10. 
 
 PLATE 39. 
 
 Fig. 40. 
 
 (MacCallum: Pneumonia in army camps.) 
 
MONOGRAPH NO. 10. 
 
 PLATE 40. 
 
 (MacCallum: Pneumonia in army camps.) 
 
MONOGRAPH NO. 10. 
 
 PLATE 41. 
 
 Fig. 42. 
 
 (MacCallum: Pneumonia in army camps.) 
 
Fig. 43. 
 
MONOGRAPH NO. 10. 
 
 PLATE 43. 
 
 Fig. 44. 
 
Fig. 45. 
 
 
 
MONOGRAPH NO. 10. 
 
 PLATE 45. 
 
 Fig. 47. 
 
 (MacCallum: Pneumonia in army camps.) 
 
MONOGRAPH NO. 10. 
 
 PLATE 46. 
 
 Fig. 48. 
 
 (MacCallum; Pneumonia in army camps.) 
 
MONOGRAPH NO. 10. 
 
 PLATE 47. 
 
 Fig. 49. 
 
 (MacCallum: Pneumonia in army camps.) 
 
MONOGRAPH NO. 10. 
 
 PLATE 48. 
 
 Fig. so. 
 
 (MacCallum: Pneumonia in army camps 
 
MONOGRAPH NO. 10. 
 
 PLATE 49. 
 
 
 Fig. 51. 
 
 (MacCallum: Pneumonia in*army camps.) 
 
MONOGRAPH NO. 10. 
 
 PLATE 50. 
 
 Fig. 52. 
 
 (MacCallum: Pneumonia in army camps.) 
 
MONOGRAPH NO. 10. 
 
 Fig. 53. 
 
 (MacCallum: Pneumonia in army camps.) 
 
PLATE 
 
 Fig. 54. 
 
 (MacCallum: Pneumonia in army camps.) 
 
MONOGRAPH NO. 10. 
 
 PLATE 53. 
 
 Fig. 55. 
 
 (MacCallum: Pneumonia m army camps.) 
 
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