there are seen nodular masses the size of a pea or cherry studding the surface and deeper structure of the spleen. This form is called Affentuberculose by the Germans, from the resemblance of the large nodules to tubercles met with in monkeys. Histologic examination proves the nodules to be composed of aggregations of tubercles undergoing caseation.

Primary tuberculosis of the spleen has never been observed. Syphilis may present itself in the form of syphilitic gummata, which are usually multiple and may be either small or large. They are distinguished by their central degeneration or by the fibroustissue striations at the exterior.

Diffuse hyperplasia of the spleen is a frequent or almost constant lesion of congenital syphilis.

THE LYMPHATIC GLANDS.

Anatomic Considerations.-The lymphatic glands consist of accumulations of lymphadenoid tissue surrounded by a connective-tissue capsule. There may be distinguished an outer cortical and an inner medullary portion, the former consisting of spherical masses or follicles of lymphoid cells enclosed in a connective-tissue reticulum springing from the trabeculæ, the latter being composed of medullary cords similar to the former in structure, but of elongated form. The afferent lymphatics enter the glands at the hilum and discharge the lymph into the cortical spheres; the liquid filters slowly toward the medullary cords, where it eventually enters the efferent lymphatics. The medullary cords are surrounded by spaces lined with endothelial cells, the lymph-spaces.

ATROPHY.

Atrophy of the lymph-glands occurs in old age and in various marasmic conditions. The glands suffer considerable diminution in size, the cellular elements being particularly affected; they are therefore hard, dry, and often irregular in shape. Fatty infiltration may occur simultaneously with atrophy, the gland in such cases preserving its size and having a decidedly fatty appearance.

HYPERTROPHY.

This is so closely allied to the conditions designated by the name of lymphadenoma that it is difficult to separate the cases which might be considered as strictly hypertrophy.

DEGENERATIONS.

Fatty infiltration is sometimes seen in cases of general obesity and also, as before mentioned, in atrophy of the glands. Amyloid degeneration is met with in cases of general amyl

oid disease, and particularly in the cases in which the intestines are affected. The lymphatic glands may, however, be independently involved in cases of tuberculosis attended with suppuration. In such instances the adjacent lymphatic glands are most likely to suffer amyloid change. The morbid process rarely leads to marked alteration of the glands, but the amyloid material may be demonstrated by the staining-reactions peculiar to it. The connective tissue of the trabeculae and around the blood-vessels is first affected; later, the endothelial cells.

Hyaline degeneration has been described. It affects the blood-vessels and connective tissue of the glands.

Calcification not infrequently forms the terminal condition in cases of necrosis or induration of the glands in consequence of tuberculous or simple inflammation. There may be small calcareous granules scattered through the gland, or the entire gland may be infiltrated.

Necrosis may occur in consequence of tuberculous or syphilitic affections, or of simple inflammation. In the former cases, particularly in tuberculosis, the center of the gland or the entire gland becomes cheesy and soft, often liquefying and discharging the contents by rupture of the capsule. In consequence of simple inflammation, as in certain infectious fevers (typhoid, diphtheria, scarlet fever), a different form of necrosis is met with, areas of the gland becoming soft, pultaceous, and sometimes putrid. The gland may rupture, discharging its contents, or absorption of the liquid with inspissation and a pseudocaseous form of degeneration may result. Finally, the degenerated area may become calcareous. Pigmentation may follow acute inflammations or traumatic

injury of the glands, the extravasations of blood occurring in such conditions leading to hematogenous pigmentation. The bloodpigment occurs in granular masses within the cells of the stroma or within the lymphatic cells themselves. Blood-pigmentation

may also occur in the glands adjacent to areas of hemorrhagic extravasation, the pigment in such cases reaching the glandthrough the lymphatic vessels and being deposited in the lymphsinuses, or even in the follicles and cords. Analogous pigmentation from external sources may result from tattooing, and occurs regularly in the bronchial glands as the result of the inhalation of various dust-particles which penetrate the walls of the bronchioles and alveoli and eventually find their way to the bronchial glands through the lymphatic stream (anthracosis) (Fig. 151). The glands may be completely black in such cases, and the lymphatic circulation through them may be obliterated. Secondary inflammatory changes result in most cases (see page 351).

INFLAMMATION; LYMPHADENITIS.

Acute lymphadenitis is commonly secondary to inflammations in the neighborhood, the irritants being carried by the afferent lymphatics. Sometimes direct extension of inflammation by contiguity of structure may lead to involvement of the lymphatic glands. Occasionally lymphadenitis is seemingly primary in cases in which the infective irritants have caused no lesion at the portal of entrance to the body.

Pathologic Anatomy.-The glands become enlarged, hyperemic, and considerably infiltrated with liquid. When the inflammation is intense there may be minute hemorrhages. Microscopically the lymph-sinuses are found distended with cells-leukocytes, red blood-cells, and proliferated and desquamated endothelial cells from the lining membrane of the sinuses. The follicles and cords are increased in size from infiltration and probably also from proliferation of the lymphoid cells. The process may become arrested and resolution to the normal condition may ensue. If mild inflammation of this character has continued for a great length of time, or if the condition is repeated, hyperplasia of the trabecular connective tissue, of the blood-vessels, and of the capsule of the gland may lead to a termination in chronic enlargement and induration of the glands.

In cases of greater intensity of the infective cause, necrotic or suppurative changes may occur. In the cases of necrosis such as occur in typhoid fever and in diphtheria there may be noted small spots of yellowish-white color in the hyperemic glands, and subsequently these undergo well-marked necrosis. Complete necrotic softening and even rupture of the gland may ensue, or, if the necrosis remains limited in extent, inspissation and sometimes calcification may terminate the process.

Suppurative lymphadenitis is not uncommon. It is seen in the glands below Poupart's ligament in cases of infective wounds of the leg; in the inguinal glands as a result of chancroid or gon

orrheal urethritis; in the glands of the neck in association with diphtheritic, scarlatinal, or other inflammations of the throat, or following erysipelas; in the axillary glands as a result of wounds of the arm; and in the internal lymphatics in various infective diseases. The term bubo is applied to suppurative lymphadenitis of superficial glands. Of particular interest is the tendency to this condition in the plague of the East, or the bubonic plague (q. v.).

Pathologic Anatomy.-The changes noted in the gland at the outset are similar to those in the simple inflammations, but under the microscope a greater accumulation of leukocytes is apparent, and the gland tends to soften, with the formation of more or less creamy pus. The capsule may prove resistant for a time, and reactive inflammation around may establish an additional wall. A single gland of a group may be affected, but more commonly the several glands are together involved. Eventually rupture may take place, but in instances in which the process has been circumscribed, inspissation of the pus and finally calcification may

occur.

In the most intense forms of lymphadenitis hemorrhagic or gangrenous conditions are developed.

Chronic Lymphadenitis leads to induration with enlargement. It occurs as the result of repeated acute attacks or in consequence of long-continued irritation by particles carried to the lymphatic glands from some focus of disease.

Pathologic Anatomy.-As a rule, the process affects the connective-tissue elements of the gland in particular, and there results a considerable amount of induration, sometimes associated with atrophy or necrosis of the proper lymphoid structure. Occasionally, however, the lymphoid elements themselves are hyperplastic, and the normal relation of fibrous tissue, follicles, and medullary cords is preserved.

Microscopically the overgrowth of the connective tissue springing from the trabeculæ, from the blood-vessels, and from the reticulum of the lymphoid portions, is apparent. This may consist of round cells and fibrous connective tissue, or there may be a tendency to the formation of epithelioid cells and even giant-cells.

Pathologic Physiology.-Inflammations of the lymphatic glands are the result of the arrest of irritants of various sorts carried to the glands in the lymphatic channels. This arrest not unlikely serves the purpose of a protection against general dissemination of irritants, and may be of great importance in this way. Complete occlusion of the lymph-sinuses by deposition of solid particles (as coal-dust), or by disease of the glands, may obstruct the lymphatic flow entirely, and a retrograde inflammatory process may result from the damming back of infected lymph or from extension of disease along the lymphatic channels.

INFECTIOUS DISEASES.

Tuberculosis of the lymphatic glands is due in nearly all cases to infection by bacilli reaching the gland through the afferent lymphatics, though occasionally it would seem that hematogenous infection occurs. Under the heading tuberculosis we must include what the older writers designated as scrofulous glands, for in the majority of such cases, if not in all, the disease is essentially tuberculosis, though the mode of infection is not always apparent. Morbid Anatomy.-The first visible change is the formation of small grayish nodules in the gland, and sometimes the eruption of these is attended with hyperemia and inflammation. Later, these tubercles increase in size and undergo caseous changes (Fig. 152) as elsewhere, and eventually the entire gland may be converted into a cheesy mass, which may liquefy and not rarely discharges through the ruptured capsule. Microscopically, the first appearance is that of gray tubercles containing giant-cells and epithelioid cells, surrounded by a zone of round cells (Fig. 153). Later, the characteristic appearances of hyaline transformation and of caseation are observed. Sometimes the glands in tuberculosis become enlarged and harder than normal, and present areas of grayish color, but do not tend so markedly to

gland (Orth).

FIG. 153.-Tuberculous lymphatic gland: a, recent tubercle with giant-cell (c); a,, inferior caseous tubercle with giant-cell (c); b, lymphadenoid tissue; d, epithelioid cell (Ziegler). undergo necrosis. In these instances the microscopic examination presents foci composed for the most part of epithelioid cells, and