Sept. 15, 1925 
Gladosporium Leaf Mold of Tomato 
529 
A, B). This mycelium so completely and thoroughly permeated the 
tissue that unstained free-hand sections gave the appearance, under 
the microscope, of a coarse reticulum of composite mycelial strands 
(pi. 4, E). This condition occurred throughout the blackened stem- 
end tissues, including pericarp, locule walls, and placentae. The 
mycelium was found considerably in advance of the margin of the 
darkened tissue, and here the intercellular strands were composed 
of fewer hyphae, more or less colorless, with longer cells of more 
uniform diameter. 
The host tissues are not immediately killed by the intercellular 
mycelium, and in fact the tissues of certain organs such as the torus 
and pedicel and even young fruits remain alive many weeks after 
invasion. In fact, the fungus seems to establish a rather nicely 
balanced parasitic relationship with its host. In the fruits, however, 
the ultimate tendency of the fungus was to mummify the tissues by 
the formation of the heavy intercellular reticulum in which the 
lumina are the host cells. Thus the affected tissue gradually attains 
a tough, spongy character. .The invaded tissues shrink or collapse 
very little because the original shape of the cells is preserved by the 
fungus reticulum. 
The hyphal aggregates were always denser and larger in the large- 
celled parenchyma surrounding the vascular bundles (pi. 3, C; pi. 4 ; 
C, P), but apparently the mycelium does not invade the bundle 
tissues proper, possibly because of the comparatively small inter¬ 
cellular spaces. This tendency of the mycelium to accumulate in the 
parenchyma around the bundles accounts for the darkened bundles 
in the torus scar and radiating out through the pericarp and placental 
tissues. In its tissue invasion the fungus apparently progresses 
most rapidly along these particular intercellular channels. In leaf 
lesions resulting from inoculations, a blackened network due to this 
accumulation of the mycelium about the smaller veins was noted 
around the margin of the killed central tissues. Makemson (8, p. 
328) also observed that the fungus in the leaves was most abundant 
around the tracheal tubes. 
The black network noted in many of the fruit lesions was due to the 
hyphal aggregates between the larger parenchyma cells of the peri¬ 
carp immediately under the epidermis (pi. 3, A, B). The dark 
radial furrows noted along the junctures of locule wall and pericarp 
in many fruits (pi. 2, E) were found to be due to similar aggregates of 
mycelium in the vicinity of underlying vascular bundles. 
The fungus appears to be strictly intercellular (pi. 4, E). Hyphae 
were not found penetrating the host cells, even in the advanced stages 
of mummification of the tissue. In young fruits the growth of 
infected tissue and the tissues supplied by infected vascular bundles 
may be retarded or inhibited, and to this is attributed the furrows or 
depressions and the one-sided growth of the fruit. In cases of the 
latter showing no dark discoloration the mycelium was usually found 
present to a greater or less extent under the torus scar, particularly on 
the stunted side. In fact, in all types of fruit infection the mycelium 
was always to be found under the torus scar, and its distribution 
could be traced outward from that point. The brown, stunted, 
placental region at the stem end of certain fruits (pi. 2, F) was found 
to be entirely mummified by the intercellular aggregates of mycelium, 
and the young ovules were also invaded and killed. 
