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Journal of Agricultural Research voi. xxm, No. 3 
With the abandonment of the theory that immunity is due to the ex¬ 
clusion of the parasite, recourse was taken to analogies with animal dis¬ 
eases, and it was assumed somewhat vaguely that resistance was due to 
“toxins and antitoxins.” 
DeBary (2) was one of the earliest workers to make careful micro¬ 
scopical studies of grain rusts. In 1866 he saw the germination of the 
urediniospores and the formation of the appressoria on the stomata. 
He noted the first flecks in six days and the earliest pustules on the eighth 
day. He also established the fact of heteroecism. 
Eriksson (7-12), in field studies of rusts, found epidemics occurring 
where there was no apparent source of infection and became convinced 
that the disease was carried in some latent and invisible form in the 
seed and the plant growing from it. He found no recognizable myce¬ 
lium in the growing plants, but thought he detected a thick plasma 
within the host cells which he believed to be a mixture of fungous and 
host protoplasm. According to him, when these infected plants approach 
maturity, the fungus ceases to be a symbiont in a latent condition and 
becomes an active parasite. The nucleus of an infected host cell becomes 
hypertrophied and represents a combination of fungous and host proto¬ 
plasm. The nucleus then partially dissolves, setting free several “cor- 
puscula nucleoli” of fungous plasm. The mycoplasm is now mature. 
The contents of these special corpuscles now pass out from the cell 
through minute pores in the wall and give rise to intercellular mycelium, 
leaving behind the empty corpuscle, which usually is elongated and sur¬ 
rounded by a broad “Lichthof.” In the primary stage of the intercel¬ 
lular protomycelial life of the fungus there are no distinctly recognizable 
rust nuclei, but in the secondary mycelium arising from the first, the 
rust nuclei are distinct. 
Eriksson’s mycoplasm theory evoked criticism and in the lively con¬ 
troversy that followed several cytological studies were published describ¬ 
ing in detail the vegetative mycelia of rusts on grains and grasses. 
Ward ( 28 , 29,30), in his account of Puccinia dispersa Erikss. on bromes, 
figured and described with great detail and accuracy the germination of the 
spore, its entry through the stoma, the substomatal vesicle, the hyphae 
growing from it, and the development of haustoria. He maintained, and 
rightly, that what Eriksson supposed to be the differentiation of myco¬ 
plasm from the intimate mixture in the host cell, and its exit into the 
intercellular spaces to form mycelium, was really the entrance of the 
fungus into the host cell to form haustoria and that Eriksson in study¬ 
ing the haustoria in all their stages exactly reversed the sequence of 
events. 
Eriksson grew grain from rusted seed in closed culture cases. A small 
percentage of the resulting plants were rusted. As no mycelium was to 
be found in the growing plants, this helped to convince him that the 
disease was propagated in latent and invisible form through the seed 
and the plant growing from it. Klebahn (18) repeated these experi¬ 
ments, using rusted seed supplied by Eriksson. No rust developed 
where the plants were kept isolated. More recently, Hungerford (17) 
grew plants from rusted seed under most carefully controlled conditions 
and obtained no rusted plants. 
Miss Gibson ( 16 ) made interesting studies of the growth of rust spores 
on plants quite unrelated to their natural hosts. The spores germinated, 
were attracted to the stoma, and usually entered and made an initial 
growth. By the end of two days, or at latest four days, the fungus had 
