or of the still surviving connective-tissue cells of the infarction, a granulation tissue is formed which gradually replaces the latter, and is changed by subsequent contraction into a scar, which in the case of hæmorrhagic infarctions may still for a long time contain pigment. The changes are otherwise, however, if the thrombus or embolus contains pathogenic bacteria, especially pyococci. There will then occur, first, a purulent softening of the thrombus or embolus, with consecutive vasculitis, and the bacteria will either soon grow through the wall of the vessel and penetrate into the tissue of the infarction, or their growth will first advance along the interior of the vessels of the latter, plugging them to a variable extent, and causing a necrosis of the vessel-wall (Fig. 111, a). Owing to the penetration of the

FIG. 111. METASTATIC INFARCTION OF THE SPLEEN IN ULCERATIVE ENDOCARDITIS. x 240. (Weigert's modification of Gram's method.) a, Branched artery with necrotic walls; b, Embolus of cocci; c, Embolus of cocci growing into the tissue of the infarction; d, Red corpuscles; e, Necrotic cells of the infarction, no longer capable of being stained.

bacteria into the tissue of the infarction, there results a formation. in it of small suppurative foci (Fig. 110, b), which by their subsequent coalescence finally change the infarction into an abscess (metastatic abscess).

Should the particles loosened from thrombi containing bacteria lodge in the capillaries or in any of the smaller-sized blood-vessels which are not terminal arteries, they will cause no infarctions, but will give rise in the neighbourhood of the occluded vessels to small rounded foci of inflammation not uncommonly bordered by a hæmorrhagic area, in which foci the tissue in immediate proximity to the

embolus is usually necrotic at the outset, while the suppuration commences at the circumference of the focus. The same effect will also be produced if the vessels affected are blocked with bacteria (such as pyococci) alone (Figs. 127, b, and 185, d). As the latter at the same time progressively increase, the vessels blocked with them take varicose forms (Fig. 127, b); and lastly the bacteria will also grow through the wall of the vessel and invade the surrounding tissue.

7. Dilatation of Blood-vessels. Aneurysms.-Dilatations may take place in arteries, veins, or capillaries, and may either extend with some regularity over a considerable section of the vessel, or else occur in the form of circumscribed protrusions. The latter are the more important, and are called aneurysms when they involve arteries.

These never form except after rupture of the coats of the vessel, whether in consequence of trauma or of faulty development or disease of the wall, and most frequently in atheroma. The rupture sometimes involves the intima, at others the middle coat or even the adventitia, different forms of aneurysm being distinguished according to these variations. The aneurysmal sac may gradually increase in size, and thus cause the atrophy of adjoining structures, including even cartilage and bone. The cavity of the aneurysm is found to contain thrombi, much stratified and sometimes of very large size, the outer layers of which are usually already decolorised. Furthermore, not only does the aneurysm in most cases show upon its internal surface the appearances of the original disease atheroma, but inflammatory growths repeatedly form in its walls, in consequence of the increasing distension, and thus cause the development of new connective tissue. In spite of this, however, the termination is, sooner or later, rupture.

A special variety of the above is the embolic aneurysm, which is developed (most frequently at the bifurcations of arteries) either through injury done to the vessel-wall by emboli with sharp angles, such as calcified particles of valves, or by the action of emboli containing bacteria, which set up an inflammation starting from the adventitia and leading to rupture of the intima or media.

It has already been mentioned (p. 204) that an aneurysm may also occur in consequence of the extension of a bacterial process to an artery from the surrounding parts.

[It is more usual, however, to distinguish a rarer form of aneurysm in which none of the coats are ruptured, and which is known in this country as true aneurysm, in contradistinction to that where one or more coats have given way, and which is termed false aneurysm. The former may be either fusiform (or tubular) when involving the whole, or sacculated when involving only a part, of the circumference of the artery. The latter is never fusiform.]-Tr.

The so-called spurious [or diffused] aneurysm is also frequently distinguished from those just described. This is formed by the bursting of all three coats and the formation by the blood-clot of a sac communicating with the lumen of the artery, the wall of which sac, however, may subsequently become fibrous by proliferation of the surrounding connective tissue.

III. LYMPHATIC VESSELS.

8. The most frequent disease of the lymphatic vessels by which of course are meant only the larger lymphatics and the thoracic duct —is inflammation (lymphangeitis), which occurs in an acute or a chronic form.

The acute inflammation is always caused by (pathogenic) bacteria, most frequently the micrococci of pus, which usually, however, merely penetrate into the lymphatic trunks from tissues already altered by them. In the former, the endothelial cells are then found in proliferation or cast off, the lumen is occupied by a fibrinous exudation or by pus, and the wall and immediate surroundings are infiltrated with small cells, whilst complete suppuration or necrosis of the wall may follow at a later period.

Chronic lymphangeitis often leads to fibrous thickening of the wall, and obliteration. Should the latter involve a large number of vessels, lymph-stasis and lymphangiectases occur in the neighbouring lymphatics, a condition which may develop not only as a result of recurring hyperamic and inflammatory conditions of the skin and subcutaneous connective tissue in elephantiasis Arabum, but also in the chyle-ducts of the mesentery after obliteration of some of them or of the thoracic duct (by inflammation or tumours).

Examination of the Circulatory Apparatus.-Brown atrophy, cloudy swelling, and fragmentation of the muscular substance of the heart are examined by tearing up fresh preparations with needles, and the examination of fatty degeneration of the heart and the walls of blood-vessels can be carried out in the same manner. Addition of dilute acetic acid or of caustic soda solution brings the pigment and fat-drops out more distinctly, while the albuminoid granules of cloudy swelling dissolve in the former. Otherwise hardening in Müller's fluid followed by alcohol, and double staining with hematoxylin and eosin or with picro-carmine (or picro-lithium-carmine) are to be recommended.

Respecting the methods of examining for fatty, amyloid, and hyaline degenerations, see pp. 53, 55, and 57--8.

The elastic tissue in the blood-vessels may be characteristically stained after the method of Herxheimer by immersing the sections (best after previous hardening in Müller's fluid and alcohol) for three to five minutes in a staining fluid consisting of hæmatoxylin, 1 grm.; absolute alcohol, 20 grm.; distilled water, 20 grm; and cold saturated aqueous solution of lithium carbonate, 1

c.cm.; after which they are extracted for five to twenty seconds in 27 per cent. perchloride of iron solution, and rinsed in water. The elastic fibres are blueblack to black, the surrounding tissue grey to bluish.

Another method (that of Manchot) consists in staining the sections in concentrated aqueous solution of fuchsin (after freeing them from celloidin), washing in water, and allowing them to lie until they have become reddish-violet in an aqueous solution of sugar of the consistence of glycerin, to every 10 c.cm. of which three or four drops of sulphuric acid have been added. Finally they are examined in a plain solution of sugar. All the tissues lose their colour when so treated with the exception of elastic fibres (and hyaline material) which remain dark red. To distinguish the blood-platelets from fibrin in the thrombi, the method of staining given on p. 75 should be used. Whilst the fibrin is stained an intense violet colour by this process, the blood-platelets remain colourless.

Mycotic processes are examined for the individual species of bacteria by the methods given under the latter head (Part II., Chapter V.). The bacteria of endocarditic vegetations may also be examined in cover-glass preparations by rubbing down the vegetations. Careful rubbing is also necessary in preparing cultures. Alcohol must be employed for hardening, and the treatment with alkaline or carbolic methyl blue adopted for sections when the bacteria are unknown or are difficult to stain.

CHAPTER III.

THE SPLEEN, THE LYMPHATIC AND THYROID GLANDS, AND SUPRARENAL CAPSULES.

I. THE SPLEEN.

1. Degeneration, Disorders of Circulation, and Inflammation.-Amyloid degeneration attacks either the Malpighian follicles (sago spleen,' which is the most frequent form), or the pulp. In the former case the arteries of the follicles are first diseased, after which the connective-tissue stroma becomes involved in the degeneration. In the second case also it is first of all the reticulum which swells up owing to the degeneration and becomes glassy, whilst the cells of the pulp usually perish by atrophy, but also perhaps partly by amyloid degeneration. The walls of the veins and capillaries of the pulp of course degenerate also.

Infarctions may be caused in the spleen, as in other organs, by either infective or non-infective emboli, and in other respects also show no deviations from the general course of events already depicted on pp. 210-213, except that in hæmorrhagic infarctions the centres of the Malpighian follicles usually remain free from extravasations.

Active hyperamia and acute inflammation of the spleen do not admit of being sharply separated from one another; they form the acute enlargement of the spleen which is usually present in acute infective diseases. In these conditions at the outset not only are the veins and capillaries found to be dilated, but many red corpuscles are also seen in the pulp spaces (Fig. 66, B). At a later stage, when the spleen becomes paler, the colourless elements of the pulp are also increased, so that we see partly small leucocytes, partly large cells with vesicular nuclei, and in which red corpuscles are often enclosed (Fig. 66, c). Sometimes also the follicles are enlarged in consequence of growth of their cells. In this stage the capsule of the spleen often shows delicate fibrinous deposits upon its surface.