presence of 16S rRNA gene in the bacterium isolated from
inoculated parents and the eggs laid by infected parent. Resultant
juvenile silkwormsacquired the bacteriumfromthe parent
for colonization through eggs. The study also revealed that, the
possible cause of increased larvalmortalityowing to pathogenic
B. subtilis during F1 progeny may be due to the progression of
infection during larval development, that ultimately lead to
death at later stages. The schematic representation of transovarial
transmission of B. subtilis in the silkworm, B.mori (Fig. 5)
suggests the progress of bacterial persistence in the silkworm
eggs. The transition period fromone stage to the next, increased
with increasing dose of B. subtilis, suggests that the severity of
disease is linkedwiththe bacterialnumber involved in infection.
The severity also extended in the fifthinstar larvae,wheremany
failed tometamorphose and never reached the adult stage