530 
Journal of Agricultural Research 
Vol. XXXI, No. 6 
Furthermore, as will be described later, the fungus invariably was 
found in the torus of infected fruits, a fact which may afford explana¬ 
tion for the observed failure of infected fruits to abscise normally. 
When infected fruits were picked, the torus usually remained firmly 
attached to the fruit and the break occurred at the pedicel node above 
the torus. 
A study of a large number of cases of sepal, torus, and pedicel 
infection showed that the mycelium was intercellular in these organs, 
and, as in the fruit, formed dense aggregates in the parenchyma im¬ 
mediately adjacent to the fibro-vascular bundles, although none 
occurred within the bundles proper (pi. 4, C, F). The mycelium 
completely permeated the cortex, pith, and interfascicular paren¬ 
chyma of the torus, but in the pedicel it was much more abundant 
in the cortex than in the pith. In general, the mycelial aggregates 
were not as dark as in the fruit and the dark stromatic bodies occurred 
less commonly. The distal portions of infected sepals were killed, 
but the tissues of the pedicel and torus apparently were not killed 
by the parasite, and infection of the latter organs could be detected 
only by microscopic examination for the presence of the mycelium, 
although tufts of sporophores were often present on large stromatic 
bodies in the stomata. Sporulation was abundant on infected 
sepals, especially on the lower surface, and the stromatic bodies bear¬ 
ing the sporophore tufts were well developed in the stomata of the 
sepals. 
MODE OF FRUIT INFECTION 
Halsted (4) reported successful wound infection with spores taken 
from leaves but did not prove the identity of the fungus in the fruit. 
He also reported one case of successful infection of the stem end of 
the fruit. Makemson {8, p. 822) proved that leaf infection by Clado- 
sporium fulvum occurs through the stomata, but he was unable to 
obtain infection of fruits, wounded or unwounded. He observed 
infection of all parts of the flower, and states that fruits the 
size of a pea and smaller were unquestionably infected. This he 
explains (8, p. 819 ) on the basis that the young ovary possesses 
stomata and lenticels which may afford an entrance to the parasite 
and that these stomata are rapidly transformed into lenticels, so 
that by the time the fruit is as large as a pea no more infection 
can occur. But careful microscopic examination has revealed 
neither stomata nor lenticels in the epidermis of young tomato fruits 
and ovaries, although stomata have been found on the style, torus, 
sepals, and pedicel. 
All attempts to produce infection by artificial inoculation of fruits 
in the laboratory gave negative or inconclusive results. Inoculation 
by puncturing fruits with a flamed scalpel dipped in a spore suspen¬ 
sion, and by placing a drop of a spore suspension about the lower 
margin of the torus or on the stem-end scar from which the torus 
was freshly removed resulted in no infection. Y+\ 
The best clue to the mode of fruit infection was afforded by the 
distribution of the mycelium within the tissues. The outstanding 
feature of the disease was the constant association of the lesions with 
the stem end of the fruit. In the few cases among the several hundred 
fruits examined where the lesion did not visibly emanate from the 
stem-end scar, the mycelium could be traced back from the visible 
lesion along the fibro-vascular bundles of the pericarp to the stem 
