132 DIE-BACK OF CHILLIES IN RIHAR 
The fungus hyphe enter the seed coat directly through the outer cellulose 
wall. The hypha, without necessarily forming an appressorium, bores its 
way through the upper wall and enters the cell cavity (Plate IJ, fig. 4). In 
badly infected seeds this upper wall has been very often found to be 
destroyed. The hypha now crosses the cell cavity and reaches the 
thickened inner walls. Here it swells at the point of contact, and from 
this swelling an exceedingly fine process is put forth which bores its way 
through, delignifying the wall (Plate II, fig. 5. As the result of delignifica- 
tion, cellulose is left. That this happens is clearly seen by the action of 
Schulze’s solution; the tunnels in the thickened walls formed by the hyphe 
take a blue colour with this reagent. 
Thus, unlike the hyphe of Macrosporium Solani Cke.,' which infect the 
tomato seed through the micropyle, the hyphe of Vermicularia Capsici 
Syd. enter the perisperm and endosperm directly through the seed 
coat. 
In the infected chilli seed there is no formation of a thick weft of compact 
mycelium between the seed coat and the endosperm, as found by Miss Massee 
in the case of the hybernating mycelium of Macrosporiwm Solani Cke. in 
tomato seeds. Even inadvanced cases of attack the testa ofthe chilli seed is 
in contact with the inner tissues except where stromatic bodies are formed 
in the cells adjacent to the seed coat which is consequently slightly lifted up 
at this place. The hyphe are septate, of variable thickness, inter- and intra- 
cellular, and hyaline, but they turn brown when they collect in masses to 
form stromatic bodies. These bodies are composed of small pseudo- 
parenchymatous cells. They are found both in the cells of the seed coat and of 
the inner tissues. Some sections of diseased seeds have shown fruiting 
pustules embedded in the inner tissues. 
An infected seed in which the embryo is not attacked will germinate ; 
but conditions suitable for the germination of the seed are also favourable for 
the dormant stromatic bodies within the seed and on the seed coat to resume 
their activities ; these stromatic bodies have been found to remain viable for at 
least a year. Therefore there is the danger of the embryo getting diseased at 
any stage of its germination as long as any part of it is within the seed coat. 
The infection may spread through the diseased endosperm or from the outside 
of the diseased seed coat to those parts of the germinating embryo in contact 
withthem. Ifthe infection takes place when the cotyledons are still completely 
1Massec, J. On the Presence of Hybernating Mycelium of Macrosporium WSolant 
Cke.in TomatoSeed. Kew Bull., 1914, No. 4, p. 145. 
