Such milk can spread

in the milk of tuberculous cows. the disease (Pl. 1, Fig. 3). The bacillus adematis maligni gives rise to malignant cedema. The bacillus of syphilis, or Lustgarten's bacillus, is not definitely determined to be the cause of syphilis. The bacillus mallei is the bacillus of glanders. The bacillus anthracis is the bacillus of anthrax, splenic fever, wool-sorter's disease, or malignant pustule (Fig. 13). The ray fungus causes actinomycosis. Streptococci are found in noma. No specific organism has been isolated for traumatic spreading gangrene or hospital gangrene; only pus cocci have been found. The bacterium coli communis is the supposed cause of peritonitis (q. v.).

II. INFLAMMATION.

Definition.-Inflammation is a nutritive disturbance arising from tissue-damage, and is not an increase of nutrition. It is defined by Burden-Sanderson as "the succession of changes which occur in a living tissue when it is injured, provided that the injury is not of such a degree as at once to destroy its structure and vitality." The changes alluded to in this definition comprise—(1) changes in the vessels and the circulation; (2) exudation of fluids and solids from the vessels; and (3) changes in the perivascular tissues.

In

Vascular and Circulatory Changes are essential to inflammation in both vascular and non-vascular tissues. the former they occur in the tissues; in the latter (cornea and cartilage) they are manifest in neighboring tissues from which the non-vascular area derives its nutritive material.

Active Hyperæmia.—When an irritant is applied to tissue, there may be a momentary arterial contraction due to irritation of the nerves, but this contraction is transitory, and is not an inflammatory phenomenon. The first vascular phenomenon is dilatation of all the vessels-capillaries,

venules, and arterioles-appearing first, and being most pronounced, in the small arteries. As a result of this dilatation. there is increased rapidity of circulation and increased determination of blood to the part. This condition of increased circulatory activity is known as "active hyperæmia" (Fig. 15).

Retardation. During active hyperæmia the capillaries are crowded with corpuscles and the blood in the veins is of a much brighter red than in health. The red blood-cells are swept along the centre of the current (in the axial stream), the white blood-cells float lazily along near the vessel-wall. After a variable time the blood-current begins to slow down until it becomes more tardy than in health.

FIG. 14.-Normal Vessels and Blood-stream: a, artery; b, vein; c, capillary (Landerer). This is known as "retardation of the circulation." Retardation is first noted in the capillaries, next in the venules,

FIG. 16.-Stasis of Blood and Diapedesis of White Corpuscles in Inflammation: a, artery; b, vein; c, capillary (Landerer).

and last in the arterioles; but arterial pulsation continues. The white cells show a strong tendency to adhere to the vein-walls, and, as a result, accumulate against the inside of, and stick to, these walls and to one another until the veins are entirely lined with layers of leucocytes. In the capillaries some leucocytes gather, but not many. In the arteries they try to adhere during cardiac dilatation, but are swept away by the force of the heart's contraction.

Oscillation and Stagnation.-By this accumulation of leucocytes the blood-stream is progressively narrowed and the axial current is impeded. The red blood-cells begin to stick to one another, forming aggregations like rouleaux of coin, which increase the difficulty the axial current has to contend with, until progressive movement ceases and the contents of the vessels sway to and fro with the pulse. This is the stage of oscillation. In a short time oscillation ceases and the vessels are filled with blood which does not move. This is known as "stasis" or "stagnation." If stasis persists, we get coagulation or thrombosis. We can then sum up the vascular changes of inflammation by stating that they consist in a dilatation of the vessel-walls, in a primary acceleration, a secondary retardation, and a subsequent stagnation of the blood-current with adhesion of leucocytes to the walls of veins and capillaries, and in the aggregation into masses of the red blood-cells (Fig. 16).

Exudation of Fluids. It is to be remembered that in ordinary nutrition serum and white cells pass into the tissues through the walls of vein and capillary. In inflammation the same thing happens, but the exudation is vastly greater in amount and is different in composition. In any slight inflammation, and in the early stages of any inflammation, there is an increase in the serous exudate, and we speak of the condition as "serous inflammation." This fluid is really not serum, but is liquor sanguinis. We find serum

in passive congestion, not in active hyperæmia. It contains very few white cells. If the inflammation goes no further, the exuded serum is drunk up by the lymphatics. A blister is an example of serous inflammation. If the inflammation continues to intensify, the exudation is altered in character-it becomes thicker, turbid, and very coagulable. It contains white cells and fibrin elements, and coagulates in the tissues. This fluid is known as "lymph" or plastic exudation, and when it is present we speak of the condition as "plastic inflammation." The lymphatics endeavor to absorb the fluid, but it occludes them by coagulation, and the area they drain becomes swollen, hard, and “branny.” This lymph can be seen in the anterior chamber of the eye in cases of plastic iritis.

Diapedesis or Migration.- Even early in an inflammation some few white corpuscles pass through the vessel-walls; but when the inflammation is well established large numbers pass, and when it is severe, vast hordes. This process is known as "diapedesis" or "migration." The leucocytes throw out protoplasmic arms, insert themselves between the cells of the walls, and pull themselves through by their amaboid movements. They do not pass through existing open doors, but form openings which close after them. This is readily accomplished, because the vessel-wall is itself damaged, weakened, and convoluted. This escape of leucocytes takes place chiefly from the venules, though some migrate through the capillaries and arterioles (Fig. 17).

In very acute inflammation the vessel-walls are so damaged that red corpuscles also escape, making the tissue appear as if infiltrated with blood. The white corpuscles greatly increase in number in the blood of a person who has an acute inflammation, and the blood-making organs, such as the spleen and lymphatic glands, are often enlarged. The blood-plaques or third corpuscles are found to be pres