DISEASES OF SILKWORMS. 



29 



of the disease; the internal signs are oval corpuscles only visible through 

 the microscope. 



Worms healthy l)orn may contract pebrine during life, but this may 

 not prevent their spinning, as the disease does not reach its climax 

 before the chrysalid or moth stage, and in its incipiency the worm is 

 strong enough to spin, though the moth will produce diseased eggs. 

 Hence the necessit}^ of repeating the microscopical examination for 

 each generation of worms. 



Pebrine is not always visible, 

 and when latent induces other 

 diseases. When onl}" one crop 

 of cocoons is made annually, it 

 is comparatively easy to resist 

 pebrine, as the germ of it, out- 

 side of an egg, retains its vitality 

 not longer than seven months. 

 The disease takes thirtj" days to 

 develop; therefore, if worms 

 from pebrinized eggs can be 

 made to spin within twenty- 

 five days after hatching, they 

 may 3aeld a fair harvest of 

 cocoons. In any case, however, 

 it is only safe to use pure eggs, 

 as pebrine, even in undeveloped 

 stages, renders the worm more 

 liable to contract all other dis- 

 eases. 



FLACHERIE, OR FLACCIDITY. 



This is now the most dreaded 

 disease among European silk- 

 worms. In general, worms are 

 struck with it after their fourth 



molt, when they are mature, or Fig. 12.-Worms affected with Aacherie dying in the 

 ,. . . . brush (after Pasteur). 



even while spinning (hg. 12). 



Without any apparent cause, they begin to languish, then remain 

 completely still, and shortly die. The}^ blacken after death (fig. 13), 

 and give out a disagreeable odor. Often entire chambers parish in a 

 day. Again, the progress of the disease may be ^ow, the worms even 

 spinning their cocoons, but, dyino- in the chrysalid state, they putrify 

 and soil the cocoon, thus greatly diminishing the value of the harvest. 

 Flacherie is but another name for indigestion. Pasteur and many 

 other scientists assert that flacherie is due to ferments and vibrioni 

 developing in the intestinal canal of the worm; other authorities main- 

 tain that the disease may exist independently of these. However, as 



