Lobular and vesicular pneumonias are usually secondary processes.

It is very important that we should understand the differences presented by the inflammatory product in regard to its plasticity, inasmuch as they are most intimately associated with the condition of the blood (the general disease). Instead of the plastic, hepatized product, we meet under various conditions with serous, flocculent, and turbid, or gelatinous and glutinous or sero-purulent, or even ichorous infiltrations, which, in consequence of their deficiency in coagulable matters, can never give rise to a granular texture of the parenchyma (hepatization). The lung adjacent to the infiltration is dense and spleen-like, and in addition to the other marks of the inflammatory stasis, is generally discolored, somewhat resistant to the touch, but on closer examination is found to be yielding, and is easily torn. Primary acute pneumonia usually deposits a plastic, hepa-tizing product, which goes through the metamorphoses which have already been described; while, on the other hand, the last-named products are often the result of sluggish, asthenic (hypostatic) inflammations, and even more frequently of secondary pneumonic processes; they represent secondary exudative processes which not unfrequently degenerate into gangrene.

One of these pneumoniac infiltrations, namely the gelatinous, must here be especially noticed. It is altogether different from the condition to which Laennec applied the denomination of gelatinous tuberculous infiltration, and which Andral, without hesitation, put down as the product of inflammation, and which we regard as the product of an inflammation of the interstitial tissue (see p. 78). In place of the plastic hepatizing product, the air-cells are found to contain a gelatinous, viscid fluid, sometimes almost resembling frogs' spawn, and of a grayish, grayish-yellow, grayish-red, or brownish-red color, and either clear and transparent, or flocculent and turbid, while the parenchyma is of a pale red tint, or more frequently of a reddish-brown color, and is easily torn. The pneumonia which deposits this non-plastic product is chiefly observed around pulmonary tubercles, and especially around infiltrated tubercles and hepatizations which are undergoing metamorphosis into tuberculous infiltration; it is developed towards the end of the disease, and sometimes involves all the parenchyma which had remained free from tubercle and tuberculous infiltration; moreover we sometimes observe it in the vicinity of extensive hepatization, especially on the border of a hepatized lung in which emphysema has been developed, and which is impervious to a dense injection. Finally, it occurs whenever there is a deficiency of plastic matter for the deposition of a coagulable, hepatizing product, either from some primary cause or in consequence of too profuse previous exudations.

Finally, we must here offer a few remarks on certain metamorphoses which constitute a hitherto undescribed termination of pneumonia, and which the plastic (fibrinous) hepatizing product of inflammation undergoes in consequence of an inherent peculiar constitution depending on a general dyscrasia. These are its very frequent conversion into tubercle in the form of tuberculous infiltration or of infiltrated tubercle, and its very rare transformation (organization) into medullary cancer, as cancerous infiltration or infiltrated cancer of the lung, to which We shall again return in our remarks on tuberculosis and cancer of the lungs.

There is a peculiar form of pneumonia to which the term hypostatic has been given by Piorry, and which is developed from the passive stasis which occurs in the most dependent parts of the lung, and to which the term pulmonary hypostasis has been assigned (see p. 59). It presents the thorough stamp of asthenic inflammation; for it is usually inert in its course, and lingers for a prolonged time in the stage of stasis, the parenchyma being of a dark livid color, and gradually developing from isolated spots a lax, soft, livid-brown hepatization, which may either be general or limited to several foci, while a considerable portion, and occasionally even the whole, may become the seat of an inflammatory product in the form of a sero-purulent or gelatino-puru-lent infiltration without a trace of hepatization. It constitutes the foundation of most of what are called latent inflammations of the lungs.