370 Wormald '. — ‘ Brown Rot ’ Diseases of Fruit Trees. 
therefore liable to infection from two sources, viz. mummied fruit and 
infected flowers. 
(3) The pustules borne by the mummied fruit became extremely 
pulverulent with conidia (the saturated atmosphere being particularly 
favourable for their development) during the period when the flowers 
were open. 
Another important factor was the great fertility of the trees during 
the previous season, in consequence of which many plums and cherries had 
remained unpicked and had become infected with Monilia , with the result 
that they persisted on the trees as ‘ mummies ’ and served as the primary 
source of infection during the spring of 1918. 
{e) Monilia cinerea and M. fructigena on Pyrus spp . 
The assumption that Monilia cinerea rarely occurs on the c cored fruit ’ 
has been negatived during recent years, the fact that this species may 
frequently cause the destruction of 50 per cent, to 75 per cent, of the 
inflorescences of certain varieties of apple trees and that it is generally 
distributed throughout the fruit-growing counties in the south of England 
being sufficient evidence that on those varieties of apple trees it is far 
more dangerous than M. fructigena. The latter species occurs almost 
exclusively on the fruit, but occasionally extends from the infected apple 
into the fruiting spur (Fig. 3) or even into the branch to form a canker 
(Fig. 14). M. cinerea , on the other hand, infects the flowers and, rapidly 
advancing into the spurs, kills them, and cankers, girdling the branches, 
are often produced (see Figs. 10-13). The statement made in 1917 that 
I had never found M. cinerea on maturing or ripe apples still holds good. 
With reference to the Brown Rot Canker disease, earlier observations 
appeared to show that the fungus produces fructifications on spurs and 
cankers during the winter and spring following their infection, and that 
subsequently the fungus produces no more pustules, but dies away, 
and the cankers become covered by the development of callus (see 
Fig. 16). More recent observations have shown that, although this is true 
as a general rule, in some instances infected spurs have developed pustules 
during the second year after infection. Thus in the summer of 1917 it 
was found that a few of the spurs labelled as being infected in 1915, and 
which had produced pustules in 1916, also bore pustules in 1917 ; in one 
instance a spur which had been infected from artificial inoculation of the 
inflorescence from a pure culture in 1916, and had borne fructifications in 
1917, produced still other pustules with viable conidia in 1918, though the 
canker which had been formed at the base of the spur was by this time 
almost healed over by callus (see Fig. 13, which shows the spur and canker 
here referred to, photographed in March, 1918). In every case observed 
where a canker has been produced that has not completely girdled the 
