BULLETIN 387 



not happen, as may be seen by examination 

 of cross-sections. Besides, if it did, it 

 would explain only the presence of longi- 

 tudinal rows of diseased cells, and not nec- 

 essarily the whole " Krankheitsherde." For 

 example, in figure 106 the original cortex 

 was five cells wide. That is the same number 

 as is found in the " Krankheitsherde." 

 These are connected by a single row of 

 diseased cells. How could the diseased 

 area have originated without direct migra- 

 tion and still show no radial hyperplasia? 



Woronin's (1878) view is that the para- 

 site, taking advantage of the pits found 

 in the parenchyma, goes directly from cell 

 to cell and thus thruout the root, much 

 like Spongospora subterranea in tubers as 

 described by Kunkel (1915) except that the 

 organism in the potato is intercellular. To 

 Nawaschin (1899), who saw no actual pas- 

 sage thru the walls, it seemed too difficult 

 a task for the amoeba to break thru the 

 plasma membrane; hence he decided that 

 there is never any migration, the distri- 

 bution being due entirely to rapid division 

 of diseased cells. 



Maire and Tison (1909, 1911) and 

 Schwartz (1910, 1911, 1914), who have 

 made observations on the other Plasmo- 

 diophoraceas, explain the scattered diseased 

 areas as due to infection of the apical cells 

 which by subsequent divisions gives rise to 

 the diseased rows so often seen. Schwartz 

 (1911), in spite of the fact that he saw 

 pseudopodia in Sorosphaera graminis ex- 

 tending thru the cell wall, makes the state- 

 ment that he does not believe species of any 



FIG. 106. FORMATION OF " KRANK- of the genera show direct migration. He 

 HEITSHERDE" explains his skepticism on the ground 



im^^d-^SeySJS'S^ed^aS that he never saw any accompanying 



in number thru outward pressure of the - . , < < 



hypertrophied ceils, x no nucleus in these pseudopodia. 



