Bark Canker Disease of Apple Trees. Grace G. Gilchrist. 233 
plant limits the progress of the fungus by the formation of 
successive cork layers, not very far distant from each other. 
In the present case, however, the cork layer is formed at very 
great distances from the old ones, sometimes 5 or 6 inches, or 
even more. A scar may progress longitudinally as much as 
18 inches at a single step, although in a transverse direction it 
rarely exceeds } inch. 
The opinion of American workers appears to be that the 
fungus is confined to the cortex and that the damage resulting 
from it is negligible. That may be so under American conditions, 
but in the case of the two outbreaks which have been recorded 
in England severe damage was being caused. It may be that 
the fungus becomes virulent when the trees are in a starved 
condition, but once it gets a firm hold on a plantation it may 
cause the loss of many trees. Not only the cortex is affected 
but also a large part of the woody tissues. 
DESCRIPTION OF THE FUNGUS. 
1. Appearance of fungus in tissues. 
The hyphae of Myxosporium corticolum are hyaline and vary 
greatly in thickness from Ip to 3-4. The mycelium is mostly 
confined to the cortex and at first does not penetrate far into 
the wood, but later penetrates as deeply as the wood of the 
second year. It grows freely in the dead tissue and is very 
abundant in the cortex and outer phloem. It is found chiefly 
in the air spaces of the cortex, but also in the cells themselves. 
In the wood the hyphae are confined almost entirely to the 
vessels and pass from one vessel to another through the pits 
(Pl. XI, figs. 13, 14 and 15). 
2. Distribution of mycelium in a mature canker. 
In its first stages the bark canker disease is essentially a bark 
disease but eventually the remaining part of the stem also be- 
comes infected. Fig. 10 is a photograph of the diseased branch 
shown in Pl. IX, figs. 2, 3 and 4, cut transversely at distances 
4cms. apart arranged in rows from below upwards. In the 
lowest section (row 1) the only sign of disease was the presence 
of two cracks in the cortex, which were evidently the cracks 
where the scar was extending and which are very clearly marked 
in fig. 4. In the second section, the cracks were more prominent 
but the tissue between them was not discoloured. The fourth 
section showed dead tissue between the cracks, although such 
tissue was almost confined to the cortex, and of course repre- 
sented the dead tissue of the old scar which had been killed 
long ago. The other sections revealed the presence of the scar 
