Bezancon's report is given in great detail in Bender's article, Gas d. h\l =o^\p., 1900, lxxii, 375, from which the following review was obtained.

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Catalase is a ferment which occurs in all vegetable and animal tissues, and is characterized by its power of decomposing hydrogen peroxide with the formation of water and the evolution of oxygen. Schoenbein in his studies on hydrogen peroxide, found that it was decomposed by extracts of animal and plant tissues obtained from the most diverse sources, and he considered that all ferments possessed the property of decomposing hydrogen peroxide, which besides was able to effect their specific activity. His experiments showed not only that some enzymes did not have the power of splitting hydrogen peroxide, but that by the addition of weak acids and other inhibitors, enzymes could be made to lose their power of decomposing hydrogen peroxide without losing their specific action, for example, by heating emulsin or by adding weak acids to it, its action on hydrogen peroxide decreased more rapidly than its action on amygdalin. This was the first indication of the specific nature of the enzyme which catalytically decomposes hydrogen peroxide, namely, catalase.The property tissue extracts have of producing a blue coloration with tincture of guaiac in the presence of hydrogen peroxide was also thought by Schoenbein to be brought about by the various soluble ferments. He obtained both of the above reactions--the guaiac blueing test in the presence of hydrogen peroxide, and the 1

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Acid administered to rabbits by intrabronchial insufflation causes an immediate and extreme damage of the lung tissue. Within certain limits the degree and extent of the injury vary according to the concentration of the acid. With the greater concentrations death occurs promptly, almost immediately, and the lethal process has associated with it a decreased permeability of the pulmonary vessels. The latter fact has been confirmed by postmortem arterial injections. With weaker solutions the results, grossly and histologically, resemble those noted after influenzal pneumonia and gas poisoning. Thus, there is destruction of the epithelium of the bronchioles, the alveolar ducts, and the alveoli. The extent of the damage to the alveolar walls varies. Exudation occurs into the alveolar, interstitial, perivascular, and peribronchial tissues. Primarily this exudate is serous, but a rapid deposition of fibrin occurs, and later polymorphonuclear leucocytes and erythrocytes accumulate. In different animals, or in different portions of the same lung, there may be consolidations of different types, serofibrinous, hemorrhagic, or purulent, with or without destruction of the alveolar walls. Subsequent changes relate to the organization of the exudate, necrosis, proliferation of the epithelium in the alveoli and bronchi, and, finally, to the regeneration of the pulmonary parenchyma. Experiments now in progress indicate that similar changes can be induced by various acids, both inorganic and organic. Experiments also show that similar changes are produced in other species of animals but that species differ in their resistance according to the acid and the concentration in which it is employed.

In our study of the histogenesis of the miliary tubercle developing inside the liver lobule in animals that have been stained vitally while inoculated with bovine tuberculosis, the controls enable us to recognize the manner in which the vital stain affects the liver. There is therefore no possibility of confusing the effects due to the organism with the effects due to the dye. It is, however, of interest to note that the effects are closely related. The vital stain alone is able to produce gradually some of the same changes that occur with far greater rapidity in experimental tuberculosis. Although in a few hours the Kupffer cells of tuberculous animals begin to react to the disease, in the case of normal animals stained vitally they do not do this until after the third or fourth dose of successive daily injections. After many days, nevertheless, the vital stain alone produces enlargement, proliferation, and separation of Kupffer cells so that these are converted into large free phagocytes which may possess one or several nuclei. These are the gigantic macrophages of chronically stained animals. In all our experiments we have used only acutely stained animals, so that the effects of the dye itself are never sufficient to produce the changes. In fact there is no evidence that the dye accentuates the changes appreciably during the time involved in the experiment. The dye, however, shows us the type of the cells entering into the tuberculous granuloma, for when fed to the body fluids in abundance trypan blue finds its way into all cells capable of receiving it. The vital stain is, as it were, a physiological test for the cells. Whatever the fundamental nature of the vital stain produced by trypan blue and the benzidine dyes may be, it is important that this reaction does not occur to any appreciable extent with mononuclear blood cells, and that it does occur emphatically in the case of the hepatic endothelium. By means of this vital test, then, the following phenomena occur when suspensions of tubercle bacilli are let into the portal blood stream. The organisms, swept on by the blood stream, finally lodge in the terminal branches of the portal vein, where they plug the vessels and continue to multiply. They injure the vessel wall and cause around them an exudative inflammatory process, and finally lead to the formation of tubercles situated not only in these areas but also within the liver lobule. The injury to the vessel wall is manifested in the early stages by the presence of vitally stained areas in its structure. The bacteria at the end of half an hour are found to be extracellular in clumps in the larger vessels, but already to some extent in the bodies of vitally stained Kupffer cells throughout the liver. Exudative inflammation manifests itself by the presence of a transitory accumulation of polynuclear leucocytes about the bacterial clumps, which may be seen as early as half an hour after the inoculation. They continue to be present in the larger cell clumps of the periportal areas for many days, but they are rapidly replaced by other cells, mononuclear in type, so that within a day the histological appearance of the portal plug has changed radically. The mononuclear cell thus entering most actively into the reaction is endothelial and not hematogenous in origin, the vital stain enabling us to make a clear distinction. This fact, evident in the portal plugs, is decisively shown in the case of tubercles developing within the liver lobule. Such tubercles probably result from the localization of individual organisms within the Kupffer cells, for the initial stages of such a probable cycle have been found by us. They consist of the occurrence of mitoses in certain Kupffer cells where the Ziehl-Nielson method shows a bacillus or several bacilli to have been phagocytized (figure 4). Rapid growth of the infected cell now takes place, and at thirty-six hours the multinucleated giant cell produced is largely separated from the other endothelium of the vessel wall. Many bacilli exist within the protoplasm of these cells (figure 5), which are especially distinguishable by their intense reaction to the vital stain. They have received trypan blue to such an excess that low power views of liver sections at the thirty-six hour stage show these cells as deep blue spots (figure 8). The origin of the giant cell from the Kupffer cell is evident not only from the above sequence and from the elective stain, but also from the fact that even when fully formed, protoplasmic strands still join it to its mother tissue,—the normal endothelium of the vessel. The strands entangle other cells in their meshes, especially mononuclear blood cells, one of which, of the polyblastic type, has homogeneous protoplasm and is not infrequently encountered in mitosis. These cells are unquestionably of importance in the lesion of tuberculosis. We have seen them abundantly in the capillaries soon after the inoculation and they also occur singly or in nests between the Kupffer cells and liver columns. They are, as a rule, free from the vital dye. They continue to be concerned in the further growth of the tubercle and with the connective tissue cells make the structure of older tubercles relatively complex. On the other hand, little complexity occurs in the structure of the young intralobular masses. The miliary tubercle formed at the end of thirty-six hours is composed of a giant cell, surrounded by epithelioid cells and by blood cells of the above polyblastic type. The giant cell and its so called epithelioid cells are electively stained and are exclusively derived from the hepatic endothelium.

1. Rabbits recovering from one attack of experimental pneumonia possess an active immunity. Such animals may subsequently withstand repeated increasing doses of pneumococci intratracheally. 2. Death may supervene after any one of subsequent injections, but it seems to depend partly upon the chronic changes in the cardiorespiratory apparatus. It may at least be said that it is usually unassociated with a septicemia which is an invariable accompaniment of fatal primary lobar pneumonia. 3. The serum from animals actively immunized by the repeated intratracheal inoculations with pneumococci may be used successfully to confer a passive immunity against the homologous organism.