92 
Journal of Agricultural Research 
Vol. V, No. s 
fields not sprayed with Bordeaux mixture; in other words, epidemics 
were started from the small areas found early in the season. The 
spread of the disease was wholly comparable to the above-described 
developments on the small plot at Madison. 
Last summer (1914) three similar infection centers were found in 
fields near Presque Isle, Me. Such a center is shown in Plate VIII, figure 2. 
The infected area is set off by a white line. The question naturally 
arises as to how these centers come into existence. Are they due to 
the planting of infected seed potatoes or to wind-blown spores? It is 
impossible to answer either of these queries positively, but in the light 
of evidence now at hand both are probable. There can be no doubt 
that seed potatoes infected with P. infesians are planted by the growers. 
This has been observed many times, and in one case 46 seed pieces in¬ 
fected with late-blight were taken from a single barrel of seed potatoes 
which were about to be planted. None of these were badly infected, 
but such specimens are more certain to produce infected progeny than 
those badly diseased, as the latter often rot in the ground. 
It may well be, therefore, that these infected centers originate from 
the infected seed, even although the originally infected shoot is not 
found. This is probably due to its rapid death after the mycelium 
reaches the surface of the soil. It soon dries up and leaves little evidence 
of its presence behind. On the other hand, it is easy to understand how 
these infected centers might be caused by wind-blown conidia, but it is 
more difficult to explain their origin without making use of the progeny 
of infected seed tubers. Although it is not definitely shown how these 
infected centers originate, in the case of the experimental plots it was 
clear that they came into existence at the same time that the infected 
shoots developed. It is also known that seed potatoes infected with 
P. infesians are planted. 
RELATION OF THE MYCELIUM IN THE SEED TUBER TO THE PROGENY 
Logical as it seems that the shoots and plants produced by diseased 
tubers should become infected in the same way as the young sprouts, 
such has not been found to be the case by a large majority of the students 
of this problem. That the mycelium in the diseased tuber may renew 
infection from one year to another was first supported by experimental 
evidence in 1861 by De Bary (1). His evidence, however, was not gen¬ 
erally accepted, and in 1876 Pringsheim (29) advanced the alternate- 
host theory. It should be recalled in this connection that De Bary 
announced the fundamental rediscovery of heteroecism in Puccinia 
graminis in 1865, which probably influenced Pringsheim (29) and many 
others in accepting the alternate-host theory as a possibility in Phytoph- 
ihora infesians , where oospores were unknown and infected tubers 
failed to produce infected plants. 
