148 
Journal of Agricultural Research 
Vol. XXIII, No. 3 
may happen while the haustorium is still small and even before the entire 
contents of the haustorium mother cell have entered the haustorium; 
or the action may be much slower, allowing full development of the 
haustorium. 
There is irregularity in the balance of forces of the interaction between 
host and parasite, for in one case the host cell is severely damaged at a 
time when the fungus is not visibly harmed, and in another the host cell 
is still normal in appearance while the fungus has succumbed. Miss 
Marryat (19, p. 136) cites a nearly parallel case. In describing the general 
effect of Puccinia glumarum (Schm.) Erikss. and Henn. on American Club, 
a variety of wheat resistant to it, she says: 
Even hyphae which have managed to put out haustori a may become filled with 
small granules and their outlines appear so faint and indistinct that they seem on the 
road to complete disintegration. The host cells in such cases often appear moderately 
healthy, but in other portionsof the leaf one may find hyphae which are still flourishing 
whilst the host cells in their vicinity are gradually dying, a response to a too vigorous 
onslaught on the part of the parasite. 
Stakman ( 26, 27) also notes variability in the struggle. 
Butler (5), in an excellent review of the literature on immunity in 
plants, sums up the evidence for a connection between acidity of cell sap 
and immunity, showing that in some diseases greater acidity favors 
fungous attack, in others it retards it, and in still others is indifferent. 
In yet other cases a change in acidity during ontogeny is accompanied by 
parallel changes in immunity. A form of wheat resistant to rust had 
more acid in its sap than the other varieties tested. 
Wheat seedlings do undergo rapid chemical changes of some sort. One 
of the fixing fluids which plasmolyzed the younger seedlings fixed them 
well a week later. There is no evidence in my work at present that would 
connect this general change with rust resistance. 
There seems little room in this particular case for the “starvation” 
theory of immunity tentatively discussed as one of the possibilities, by 
Ward (28-36), Marryat ( 19), Gibson (16), Spinks (25), and others. At 
every point of entry into a host cell the fungus is either killed back or 
driven back for a short distance. When the reaction of the host is some¬ 
what deferred, the fungus makes a haustorium, and it evidently extracts 
food from the host—enough at least to let it grow on to new cells—and 
there is no evidence that this food is of an unsuitable nature. Here in these 
slower reactions we have, too, at least a hint that the harm done by the host 
to the fungus is due to a chemical reaction initiated after the entrance of the 
fungus into the host cell. The increased turgor of the host cell following 
its entrance points in the same direction. To be sure the fungus sooner 
or later exhausts itself in these unsuccessful attempts to enter into food 
relations with the host, but the observations recorded here suggest that 
in this case at least the failure of the fungus is due not so much to lack 
of proper food in the host as to a specific reaction set up there which de¬ 
stroys the fungus. 
Ward (28-30), Marryat (19), Gibson (16), Orton (21), Stakman (26, 27), 
and others favor the theory that immunity in plant diseases is due to 
antagonistic reactions between host and parasite analogous to the forma¬ 
tion of specific toxins and antitoxins in animal diseases, and the limited 
evidence presented here is in line with this. 
