Apr. 15, i9« 
Bacterial Spot of Tomato 
149 
rule, inoculation of ripe fruit has been unsuccessful. It seems plausible 
that the increase in hydrogen-ion concentration as the fruit matures 
may increase its resistance to infection. 
PATHOLOGICAL ANATOMY 
Leaf lesions were fixed in alcohol, embedded in paraffin, sectioned, and 
stained with Ziehl’s carbol fuchsin. The intercellular spaces of the pali¬ 
sade and mesophyll tissue are seen to be packed with bacteria (PI. 28, C). 
Apparently as a result of collapse of the host cells, these cavities become 
greatly enlarged and the host cells are more or less displaced by the 
masses of bacteria. The epidermis may finally become puffed outward 
as a result of the pressure produced. The subsequent sunken character 
of the lesion is attributed to the drying out of this mass of bacteria and 
killed host tissue. The silvery appearance of sunken cotyledon lesions 
is attributed to the presence of air under the epidermis after the diseased 
tissue has dried and shrunken. 
Infected leaf areas were cleared in acetic acid and alcohol, or in chloral 
hydrate, and stained with carbol fuchsin. In surface view the lesions are 
clearly visible each as a deeply stained, lacelike pattern (PI. 28, A). This 
indicates that the bacteria are in the intercellular spaces. The margin is 
composed of irregular extensions due to advance invasion of the inter¬ 
cellular spaces. The veins offer no obstacle to the progress of the inva¬ 
sion. 
Hand sections of fruit lesions show an abundance of bacteria in the 
intercellular spaces. Fruit lesions were fixed and stained with the triple 
stain or with carbol fuchsin. Very young lesions may be distinctly 
sunken on account of the collapse of the outer mesocarp cells. Older 
lesions are seen to be distinctly elevated at the center, apparently as a 
result of hypertrophy and hyperplasia of the underlying mesocarp cells 
(PI. 27, B, C). Such lesions often show a sunken peripheral zone, due to 
the collapse of the host cells. A layer of cells with suberized walls is 
formed directly underneath the necrotic tissue of the center of the lesion 
(PI. 27, B). Usually the epidermis has sloughed off from this disinte¬ 
grated tissue which is composed of collapsed host cells and bacteria. 
Large cavities packed with bacteria are visible here and there. In Plate 
27, A, the large cavity may represent the original wound through which 
infection occurred. 
Apparently the cork layer is not always an effective barrier to the in¬ 
vasion, since lesions often are deep and craterlike. Tangential invasion 
of the small-celled mesocarp tissue seems to be more active than radial 
penetration of the large-celled mesocarp tissue. 
