few days. I use no special diet in my cases and no treatment other than the serum. After the fever subsides, the patients usually have a good appetite and the prolonged, anemic, debilitated. condition, following the conventional treatment, does not occur. One thing is essential: this serum treatment should not be used as a last recort-after everything else has failed, if the best results are to be expected.

Among the patients treated with the serum, I have had three relapses. One occurred one year after the first attack. Six doses of serum were required in the 'relapse to effect a cure. It is now nearly two years since his last attack. In the second case, the relapse took place eight months after the first attack. The patient came to my office requesting a repetition of the serum treatment. One dose of 10 c. cm. was all that was required. In the third case the relapse occurred two weeks after the first attack. This is the case referred to with the neart complication.

In chronic cases, where there is a distinct history of the condition having started with an acute attack which confined the patient to bed, the serum treatment is uniformly beneficial. The beneficial results may not be apparent at the start, but if the patient is brought under the influence of the serum, improvement will come. There is a distinct tendency on the part of the patients to continue to improve for months after the treatment has been discontinued. Chronic cases where there is no fever, do not tolerate the serum as well as acute cases, the serum producing disagreeable urticaria, if the treatment is continued. For this reason it should be given at intervals of from two to three days, in 10 c. cm. doses.

1. J. A. M. A., Jan. 31, 1903. 2. Am. Med., Jan. 1, 1901. 3. Med. News, April 15, 1905.

When much swelling is at the point of injection the serum should be withheld for a week or more. After a patient has once had a serum-urticaria, he becomes very sensitive to subsequent injections, sometimes one dose of 10 c. cm. being sufficient to product the rash. These urticarias are always associated with joint-pains and some fever. Where a patient becomes sensitive to the hypodermic use of the serum it should be given per rectum, but in larger and more frequent doses. The treatment should be kept up for months, according to the nature of the case. In one case, I gave the serum at intervals for a year. This was a case of five years' standing and very much crippled. The patient's suffering from repeated relapses has been stopped and her crippled condition very much improved. No beneficial results were obtained in three cases of true arthritis deformans in which the serum was used. In one case of muscular rheumatism no results were obtained.

From a few articles in medical journals it appears that some clinicians are still contending against the infectious nature of acute articular rheumatism. The efficacy of the serum treatment, as demonstrated by actual clinical results, should, it seems to me, be conclusive evidence as to the infectious nature of the disease.

In conclusion, I would say that the results thus far obtained are (a) a material shortening of the course of the disease, (b) no relapses into the chronic state, (c) heart complications diminished in frequency or more often entirely prevented and (d) chronic cases much improved with a distinct tendency to complete recovery.

4. Med. Record, May 6, 1905. 5. Am. Med., Jan. 27, 1906. 6. J. A. M. A., April, 1903.

E. C. Yarborough, Detroit, stated that it has been his observation that all these cases, both acute and chronic, are benefited by the serum treatment. Very recently he saw one of Dr. Sherman's patients who had been a cripple for years. There were flexion and ankylosis at the knees. The patient was unable to rise from the

sitting posture without assistance. Following treatment, flexions lessened so that her crutches had to be lengthened 41⁄2 inches.

G. H. Sherman, Detroit, in conclusion, said that his experience convinced him that serum treatment had no bad effects and very much in its favor.

Pathologically there are three different and distinct types of pneumonia: Lobar, Broncho-, and Chronic Fibroid.

LOBAR PNEUMONIA.

Lobar pneumonia is an infectious disease with certain definite and constant pulmonary lesions, which develop in a well-defined course. The first stage is one of simple hyperemia, obviously very difficult to demonstrate pathologically. Hyperemia of the lung is only a relative condition at most, and that condition changes within varying limits after death. Then, too, there are very few patients, indeed, who die during this primary congestive stage. At this time the lung is of a bright red color modified by the normal pigmentation-anthracosis, etc.

The engorgement increases, the pleura loses its luster, and minute hemorrhagic infarcts, or extravasations of blood make their appearance. Upon section, the lung resembles the spleen in consistency and appearance, whence the commonly applied term, splenization. Blood and air follow the knife which meets with no resistence. Crepitation of the lung substance is undiminished, and pieces when thrown into water float

*Read before the Calhoun County Medical Society, at Battle Creek, September 4, 1906.

at a slightly lower level than normally. Microscopically some of the capillaries -those of the pulmonary set-are seen to be distended, and the epithelium lining the air vesicles is slightly swollen. As this condition continues for a few hours the capillaries are widely distended, the epithelium more swollen, and some is beginning to exfoliate, with the accumulation in the air vesicles of a few epithelial cells, many leucocytes, and some serum that is beginning to filter through the distended capillaries.

When the air cells are filled by these cast-off epithelial cells, leucocytes and erythrocytes, which also pass through the vessel walls by the process of rhexis, and by the fibrinous exudate, the fibrin is deposited, consolidating the whole mass and binding the contents of the adjacent vesicles together by the passage of fibrous strands through minute holes in the walls called stomata, then we have the second, or stage of red hepatization, the mass being red from the presence of so many erythrocytes, the name significant of the close resemblance to the liver on section, both in consistency and gross appearance. The cut surface looks and feels granular, due to the projection of the plugs of fibrin which fill the air vesicles and bronchioles. These plugs are easily removed

by the edge of a knife, carefully scraped over the cut surface. Crepitation is entirely absent now, showing the absence of air, and the tissue sinks rapidly when placed in water.

During this time the pulmonic capillaries have become occluded by thromboses which gradually force their way back toward the larger pulmonary arteries and the heart, and no blood is passing through this diseased portion of the lung for purposes of aeration. The other set of capillaries, the pneumonic, which carry the systemic blood for purposes of nutrition, are but slightly, if at

The red pigment is gradually absorbed from the blood cells imprisoned in the consolidated mass; leucocytes accumulate in great numbers; and fatty degeneration sets in, producing gray hepatization, so named from the color assumed. The tissue becomes soft and uneven in color, giving a mottled appearance. A small amount of proteolytic enzyme has been produced from the breaking down of leucocytes, which has just begun, and this dissolves the fibrin so that it cannot be demonstrated microscopically. Gray hepatization is in reality only the beginning of resolution.

all, affected, as is shown by the fact that the lung tissue is well nourished, and continues so except in those rare cases in which gangrene develops, and that only follows the occlusion of this pneumonic circulation to the part.

Usually at this time the pleura adjoining the diseased lobe, and often that more distant, is covered by a dense, hard, fibrous layer which may be as much as an inch in thickness, and may bind the visceral to the parietal pleura. The affected area of the lung, if of any considerable size, will now show the impression of the ribs.

The term purulent infiltration, often. applied to the lung in the condition just described, is a misnomer, for there is no true pus present, except in isolated cases when a secondary purulent infection has occurred. The pus-resembling material is a fatty, granular detritis.

By the increased breaking down of the leucocytes, proteolytic enzymes are now formed in great profusion, which together with the process of fatty degeneration, softens the consolidated mass, liquefies it partially, and it is removed by the lymphatics, by the blood, and by expectoration. This process is called

resolution, and continues until recovery is complete. The thrombotic material in the pulmonary circulation is gradually absorbed by the blood, being rendered soluble by the action of proteolytic enzymes produced as before described. The epithelium covering the walls of the bronchioles and the air vesicles is regenerated, and the lung resumes its normal appearance, so that after recovery it is impossible to tell from microscopical examination that the disease has been present.

The

Resolution is sometimes delayed, making a long, slow process. Much speculation has been advanced to account for this condition, but recent observations by H. W. Cook in the laboratory of Johns Hopkins Hospital, on the nitrogen elimination of pneumonia patients, show that this is very high during resolution, and continues so in the cases of delayed resolution until it is completed. nitrogen comes undoubtedly from the increased excretion required by the removal of the consolidated mass in the lungs. The persistent high percentage of nitrogen eliminated would seem to indicate that there is a continued exudation, rather than simply a delay of resolution. If the latter were the case it would be impossible to account for the large amount of nitrogen eliminated.

The processes of lobar pneumonia as above outlined do not occur as distinct and separate stages, but merge one into the other. A section from such a lung will often show two and sometimes three stages of the process in adjacent fields of the microscope. Neither do these processes occur with any distinct regularity as to time-the whole process, clear through resolution, may take place in three days. Holt has seen a lung in the twenty-sixth day of the disease and resolution not yet set in. Coplin reports a case in the stage of red hepatization the thirty-ninth day from the initial chill.

BRONCHO-PNEUMONIA.

Whatever the etiology of bronchopneumonia, whether it is a primary or a secondary disease (the text books say it may be either), the pathology is that of the extension of an exudative inflammation from the bronchi, and bronchioles. First there is simple engorgement of the capillaries of both pulmonary and pneumonic circulations, which is very marked; then follows a swelling and exfoliation of the epithelial lining of the bronchioles and air cells, and exudation of serum, which may contain fibrin, but usually does not. Leucocytes pass into the air cells by diapedesis.

This inflammatory process passes along the bronchi, and through their walls, affecting the air vesicles adjacent, whether terminals of the diseased bronchus or not. The terminal air cells are affected from a bronchus if the inflammation extends that far, which is often the case in a well developed

broncho-pneumonia. When the terminal cells are not affected, they may collapse or not, depending upon whether the contained air is removed.

Engorgement, red and gray hepatization, and resolution occur in bronchopneumonia, but not in such well-marked routine, not so well defined, nor so regularly as in lobar pneumonia. The exudate does not solidify, owing to the lack of fibrin.

Near the diseased part, the lung shows compensatory emphysema-a dilatation of the air cells, with atrophy and rupture of parts of their walls and the loss of

disturbances. The vessels are enlarged, and surrounded by leucocytes which are infiltrated into the tissues, the walls become swollen and edematous due to the exudation of serum, and the connective tissue and epithelial cells begin to swell and become somewhat granular. The process extends into the air cells adjoining, which, with the pronchi, are filled gradually with a mucoid serum containing the exfoliated fatty and granular epithelial cells in great numbers, compared to lobar pneumonia. Leucocytes and a very small number of erythrocytes, also collect in the exudate.

their elasticity. The adjacent pleura is thickened and shows minute hemorrhages, caused by the excessive engorgement. These hemorrhagic areas, together with the close proximity of diseased and healthy lung, give the whole a mottled appearance.

The lower lobes on the posterior aspect, are the usual seats of disease in the commencement of the affection, but the anterior aspects of the upper lobes are often the site of selection; however, any or all lobes may be involved to a greater or less extent.

Microscopically the epithelial walls of the bronchioles first show inflammatory