50 CAUSE AMI NATURE OF CROWN-GALL 



After the plasmodium consumes the cytoplasm of the cell its- 

 visible effect may be observed upon the cell nucleus (see Plate). 

 At first the nucleus swells to from three to six times its normal 

 size, becomes less dense, and loses to a degree its normal fibril- 

 lar structure. At the same time the reticulum of vacuolar, 

 frothy protoplasm in the cell becomes more abundant and ap- 

 parent. (This condition and subsequent stages can be observed 

 in fresh specimens if a drop of Flemming be run under the 

 cover-glass a few moments before making the observation.) 

 The nucleus now loses its normal form and appears as if eroded 

 on the surface, and later gradually disappears as an organized 

 body, vacuoles frequently appearing within its ill-defined 

 margin. 



The nucleoli are the last of the cell contents to succumb to 

 the action of the parasite. In well stained sections they can 

 frequently be observed in the cell long after every other visible 

 trace of the nucleus has disappeared. Associated with the 

 nucleoli in the enlarged nuclei are usually several small spheri- 

 cal bodies which take the safranin stain. These red bodies also 

 remain behind after the body of the nucleus has been destroyed. 



The protoplasmic reticulum of the parasite contains small 

 spheroidal bodies ^ <>■ or less in diameter, which take the 

 safranin stain. These bodies are surrounded by hyaline areas 

 and are believed to be the nucleoli of the nuclei of the plasmo- 

 odium, the hyaline area surrounding each nucleolus being 

 the body of the nucleus. They are frequently in pairs and in one 

 instance appeared as if in process of division by karyokinesis. 



The cytoplasm of the plasmodium passes from cell to cell 

 through the wall pits. The unequal growth of the cell tissue 

 in closely adjacent regions soon causes the development of large 

 intercellular spaces. Occasionally a strand of protoplasm is ob- 

 served to stretch across one of these spaces joining the plas- 

 modium in adjacent cells, the communication between the two 

 cells being continued after the cells have pulled apart. 



From the position of the diseased cells in relation to the 

 meristematic tissue and the formation of new centers of such 

 tissue, it is evident that the parasite stimulates growth not so 

 much in the cells visibly affected as in adjacent ones. I have 



