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are concerned, are practically identical, are due to the action of two distinct
fungal organisms which are not even remotely related to one another !
But if there be no satisfactory ground for believing that the fungal elements
of the two commonly recognised varieties of the disease are in any way related to
one another, and if a third variety is present in which fungal elements are entirely
absent, surely the evidence for the primary fungal origin of the affection is hope-
lessly defective. Even in Mr. Kanthack's specimens of the white variety of the
disease fungal elements were absent from some of the concretions. Being con-
vinced, as he was, of the identity of the fungi in both ordinarily recognised
varieties, he not unnaturally ascribed this to antecedent degeneration of fungal
elements which had been previously present, but such an explanation is not ap-
plicable to cases where the disease is present and fungal elements are entirely
absent. When it is taken into account that the fungal elements associated with
the disease are of two perfectly distinct types, that those present in the black
variety constitute sclerotioid masses, that fungal elements are not invariably
present in the concretions of the white variety, and, finally, that a third variety
exists in which concretions and fungal elements are alike absent, can it be logi-
cally maintained that the disease has a primarily hyphomycete origin ? It may be
primarily of parasitic origin, but there is assuredly nothing satisfactorily to de-
monstrate that the recognised forms of fungal elements usually associated with
it play the part of specific primary causes.
Judging from the appearances present in a very large series of preparations,
by the generally accepted fact of the essential differences in the characters of the
concretions present in the two commonly recognised varieties of the disease, and
by the entire absence of such bodies in what there appear to be good grounds
for recognising as a third variety, I believe that the evidence points to the fol-
lowing sequence of morbid processes in the development of the disease. At the
outset we have to deal with morbid changes which are confined to the smaller
arterioles and capillaries and which lead on to more or less complete obliteration
of their lumina. In the capillaries an excessive proliferation of endothelium occurs,
so that in stained preparations the course of individual branches may be traced
almost as distinctly as though they had been injected owing to the accumula-
tions of nuclei which they come to contain (Plate I, Figs. 1, 2, 5 ; Plate II,
Fig. 6). As the proliferation of endothelial elements advances the cells no
longer form a single layer, but become stratified, and ultimately form a plug
which obstructs the lumen of the vessel and converts the latter into a solid cord.
In the case of the arterioles similar processes go on and at the same time the
muscular coat becomes abnormally thickened, whilst, with less uniformity and in
minor degree, a certain amount of hypertrophy also takes place in the connective
tissue of the outer coat (Plate I, Figs. 3, 6 ; Plate II, Figs. 5-7). Whilst these
primary changes are advancing in the vessels other morbid phenomena begin