504 BULLETIN 347 
of the chestnuts has had considerable to do with its development and 
spread*in this State. The writer more than any one else has advocated 
this view, and we propose to give here the reasons we have for holding 
it. Briefly expressed, they are as follows: 
“The chestnut blight was brought to sudden prominence just after 
the severe winter of 1903-1904, which injured and killed fruit and forest 
trees in general along the coast and watercourses, of which New York 
City was the central point. The resulting enfeebled condition of the 
chestnut enabled the blight, a previously inconspicuous parasite, to spring 
into sudden prominence on these trees and to gain credit for the death 
of others which had been largely or entirely due to winter injury. Since 
then we have had one or two severe winters, and more especially several 
dry summers, that have injured not only the chestnut, but other forest 
trees over an extended area. Due to its successful attack on the weakened 
trees, the blight fungus has perhaps acquired an added virulence that 
has enabled it to attack apparently healthy trees, especially those. of 
sprout renewal. The enfeebled condition of the chestnut trees and their 
consequent susceptibility to the blight may possibly be related to some 
lessened chemical activity in the bark and newly-formed wood, such as 
the production of tannic acid, for instance. If so, then when this has 
returned to its normal production through favorable weather conditions, 
the blight should gradually become correspondingly less aggressive.” 
Opposed to these views we have those of Metcalf and Collins (1910): 
“A debilitated tree is no more subject to attack than a healthy one. 
[See also Metcalf, 1910.] Dry weather checks the disease by suppressing 
spore production. . . . Winter injury is not common over the whole 
range of the bark disease, but may be locally important in producing lesions 
through which the parasite enters. Winter injury bears no other relation 
to the bark disease.’ Metcalf (1912 a:225) writes: ‘‘ No definite evi- 
dence, experimental or otherwise, has been adduced to show that a tree 
with reduced vitality is more susceptible to infection, or that the disease 
spreads more rapidly in such a tree than in a perfectly healthy and well- 
nourished tree of either seedling or coppice growth, provided that such 
reduced vitality does not result in or is not accompanied by bark injuries 
through which spores can gain entrance.” (See also Metcalf, ror2b: 
79-82.) The writers think that in the above quotation Metcalf has well 
summed up the apparent fallacies in the preceding statements made by 
Clinton. : 
By observations the writers have found no connection between any 
ecologic conditions and any variation in the susceptibility of the tree. 
However, ecologic conditions may determine the rapidity of spread of the 
fungus through the infection courts opened up, such as winter- and 
