Report on the Pathological Anatomy of Pleuro-pneumonia. 201 
systems, chokes their lymph-passages, and thus protluces in- 
terlobular exudation throughout the territory from which they 
come. There is no difficulty in working out a great variety of 
ways in which the disease may lie spread through the lung by 
means of the peribronchial lymph-vessels, on the one hand, and 
those under the pleura on the other ; the former leading the 
infective process to the root of the lung, the latter extending it 
over the surface of the organ. Thus the soft translucent form 
I of exudation may be spread in two ways, viz. by the subpleural 
and by the peribronchial lymphatics. This would sufficiently 
account for its irregular outline and indefinite distribution. 
But, even admitting that the irritative change in the peribron- 
chial tissues is the cause of the thrombosis and consequent 
infarction, and that it also takes a great share in the production 
of both forms of solidity of the lung parenchyma, we have made 
but little way towards finding out the starting-point of the 
disease. The occurrence of the peribronchial exudation remains 
to be accounted for, and its exciting cause must be discovered 
before we can speak of the first step in the morbid processes, 
without which the life-history of the disease is deficient in the 
most vital point. 
There seems every reason to believe that this is a process 
which goes through the same series of events as chronic in- 
flammation, such as would follow any form of persistent irrita- 
tion, and lead to intense induration. It is needless to go into 
the much-vexed question whether this be an inflammatory disease 
or not ; authors differ not only amongst themselves, but even 
with themselves, upon this point. We only know inflam- 
mation as a certain series of phenomena occurring in a certain 
order. We meet these same phenomena in the same order in 
pleuro-pneumonia, and we must find a more satisfactory ex- 
planation of its peculiarities and divergence from ordinary 
inflammation than the simple statement that it " is not inflam- 
matory in any of its stages, and never presents any of the 
phenomena which are associated with inflammation." 
In the parts where the peribronchial exudation is most firm, 
and the tissue most densely infiltrated with new cells, the proper 
walls of the air-tube are invariably much thickened, and show 
signs of long-standing disease. The lining membrane of this 
part of the bronchus is also quite destroyed by a process of 
ulceration, the epithelium cells being cast off, and forming part 
of the plug which fills the calibre of the tube. 
In those cases where there has been but little time for the 
disease to spread by the lymphatics, the destruction of the 
mucous membrane is more extended than the thickening of 
the peribronchial lymphatics. In short, the mucous membrane 
II 
