476 PROCEEDINGS OF THE ACADEMY OF [^lav, 



transversely or obliquely cut hyphse which, by their presence, stimu- 

 late the cambium to increased activity. AVith the exception of 

 these there seems to be no other attributable cause for the formation 

 of the swellings, because the wood at this stage of the disease is free 

 from all appearance of disintegration. It is, however, otherwise 

 when the disease has progressed for some years. One remarks this 

 on studying the sections of a canker that has progressed in develop- 

 ment for some ten or more years. In all of the larger swellings 

 studied by the writer, the cambium had been killed in a number of 

 places. The dead spots vary in size in different cankers, but they 

 seldom become confluent by extending completely around the stem 

 or branch. When they meet so as to girdle the stem, the stem 

 dies. More often the dead area is f-niall, remaining about the s-ame 

 size for a number of years. The living cambium makes an effort to 

 repair the damage, but this it is not able completely to do on 

 account of the presence of the mycelium in the tissues. A cavity 

 or pocket finally results at the dead spot with the increase in num- 

 ber of the annual rings (fig. 14). As with the disease of Abies 

 balsamea described by Anderson, often several such cavities are 

 formed when the cambium has been killed at more than one spot, 

 and these cavities or pockets contain hardened I'esin. In the white 

 cedar a comparatively small amount of resin collects, but in Abies 

 balsamea the amount is quite considerable. In stems of white 

 cedar that have been long diseased and that are dead above the 

 swelling the brown bark cracks off, exposing the wood, the exter- 

 nal surface of which is ventricose (fig. 14). The sap-wood of 

 such badly diseased swellings has become porous, partly rotten and 

 divided up into plates by the pores, the cracks or the fissures that 

 abound. The heart-wood is still firm. Under the microscope this 

 breaking down of the sap-wood does not seem to follow an absorp- 

 tion of the middle lamella of the cell wall by ferment action, but is 

 due to a springing free of the lignified portion of the cell wall. 

 Later the walls seem to break across and pieces of lignified cell 

 wall, some U-shaped, some Y-shaped, hang free along the edges of 

 the fissures thus formed. Here the disease has progressed to its 

 fullest extent (fig. 32). 



The hyphse from the point of infection grow through the cortex 

 and then spread vertically up and down through the phloem. By 

 the second year they have established themselves in the cambium 



